Risk Profile:
Toxoplasma Gondii in
red meat and meat products
MPI Technical Paper No: 2015/08
Prepared as part of a New Zealand Food Safety Authority
contract for scientific services
ISBN No: 978-0-908334-11-7 (online)
ISSN No: 2253-3923 (online)
January 2008
Client Report
FW06106
RISK PROFILE:
TOXOPLASMA GONDII IN RED MEAT
AND MEAT PRODUCTS
Dr Stephen On
Food Safety Programme Leader
Dr Rob Lake
Project Leader
Dr Lynn McIntyre
Peer Reviewer
DISCLAIMER
This report or document (“the Report”) is given by the Institute of Environmental Science
and Research Limited (“ESR”) solely for the benefit of the New Zealand Food Safety
Authority (“NZFSA”), Public Health Services Providers and other Third Party Beneficiaries
as defined in the Contract between ESR and the New Zealand Food Safety Authority, and is
strictly subject to the conditions laid out in that Contract.
Neither ESR nor any of its employees makes any warranty, express or implied, or assumes
any legal liability or responsibility for use of the Report or its contents by any other person or
organisation.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
January 2008
ACKNOWLEDGMENTS
The authors would like to thank Murray Wilkins, AgVax; and Sue McAllister, University
of Otago for helpful discussions.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
January 2008
CONTENTS
SUMMARY .......................................................................................................................... 1
1
INTRODUCTION .................................................................................................... 3
2
HAZARD IDENTIFICATION: THE ORGANISM.............................................. 6
2.1
Toxoplasma gondii.............................................................................................. 6
2.1.1
The organism ............................................................................................. 6
2.1.2
Growth and survival .................................................................................. 7
2.1.3
Inactivation (CCPs and Hurdles)............................................................... 8
2.1.4
Sources ...................................................................................................... 9
3
HAZARD IDENTIFICATION: THE FOOD ...................................................... 11
3.1
Relevant Characteristics of the Food: Red Meat and Meat Products ............... 11
3.2
The Food Supply in New Zealand .................................................................... 12
3.2.1
Imported food .......................................................................................... 12
4
HAZARD CHARACTERISATION: ADVERSE HEALTH EFFECTS........... 14
4.1
4.2
4.3
4.4
4.4.1
4.4.2
5
EXPOSURE ASSESSMENT ................................................................................. 19
5.1
5.1.1
5.1.2
5.2
5.3
5.3.1
5.3.2
5.3.3
5.3.4
5.3.5
5.3.6
5.4
5.4.1
5.4.2
6
Symptoms.......................................................................................................... 14
Types Causing Disease ..................................................................................... 17
Dose Response .................................................................................................. 17
High Risk Groups in the New Zealand Population........................................... 17
Pregnant women ...................................................................................... 17
Immune compromised ............................................................................. 17
The Hazard in the New Zealand Food Supply.................................................. 19
Test methods............................................................................................ 19
Toxoplasma prevalence in livestock animals in New Zealand................ 19
Food Consumption: Red Meat and Meat Products ........................................... 21
Qualitative Estimate of Exposure ..................................................................... 23
Number of servings and serving size....................................................... 23
Frequency of contamination .................................................................... 24
Predicted contamination level at retail .................................................... 24
Growth rate during storage and most likely storage time........................ 24
Heat treatment ......................................................................................... 25
Exposure summary .................................................................................. 25
Overseas Context .............................................................................................. 26
Seroprevalence in animals....................................................................... 26
Prevalence in animal tissue ..................................................................... 27
RISK CHARACTERISATION............................................................................. 30
6.1
Adverse Health Effects in New Zealand........................................................... 30
6.1.1
Incidence and outbreaks .......................................................................... 30
6.1.2
Clinical consequences of toxoplasmosis infection and people with AIDS34
6.1.3
Case control studies and risk factors ....................................................... 34
6.2
Adverse Health Effects Overseas...................................................................... 34
6.2.1
Incidence.................................................................................................. 34
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
January 2008
6.2.1.1 USA................................................................................................... 36
6.2.1.2 Europe ............................................................................................... 37
6.2.1.3 Australia............................................................................................ 37
6.2.1.4 Worldwide data for seroconversion during pregnancy..................... 38
6.2.2
Contribution to outbreaks and incidents.................................................. 39
6.2.3
Overseas studies ...................................................................................... 40
6.2.4
Risk assessments overseas....................................................................... 42
6.3
Estimate of Risk for New Zealand.................................................................... 44
6.4
Risk Categorisation........................................................................................... 44
6.5
Summary ........................................................................................................... 45
7
RISK MANAGEMENT INFORMATION .......................................................... 46
7.1
Relevant Food Controls .................................................................................... 46
7.1.1
EFSA Review .......................................................................................... 46
7.2
Economic Costs and Burden of Illness ............................................................. 48
7.3
Other Transmission Routes............................................................................... 49
7.3.1
Toxoplasma in non-livestock animals in New Zealand........................... 49
7.3.2
Prevalence of T. gondii in cats overseas.................................................. 49
7.3.2.1 The development of T. gondii vaccinations for cats......................... 50
7.3.3
Risk communication ................................................................................ 50
8
CONCLUSIONS..................................................................................................... 52
8.1
Description of Risks to New Zealand Consumers ............................................ 52
8.1.1
Risks associated with red meat and meat products ................................. 52
8.1.2
Risks associated with other foods............................................................ 53
8.1.3
Risk Assessment Options ........................................................................ 53
8.2
Commentary on Risk Management Options..................................................... 53
8.3
Data Gaps.......................................................................................................... 53
9
REFERENCES ....................................................................................................... 54
APPENDIX 1: CATEGORIES FOR RISK PROFILES............................................... 69
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
January 2008
LIST OF TABLES
Table 1:
Table 2:
Table 3:
Table 4:
Table 5:
Table 6:
Table 7:
Table 8:
Table 9:
Table 10:
Table 11:
Table 12:
Table 13:
Table 14:
Table 15:
Table 16:
Table 17:
Table 18:
Livestock numbers, production and export for New Zealand .............................12
New Zealand domestic meat consumption per capita 1985, 1995, 1996, 1999 to
2006 (kg/person/year) ..........................................................................................21
International comparison of meat consumption, 2003 (kg/person/year) .............21
Mean estimates of New Zealand domestic meat consumption in 1997 and
estimates of meat available for consumption, 2004.............................................22
Types of red meat and meat products consumed, by servings and by weight .....23
Data for meat and poultry cooking preferences in New Zealand ........................25
Reported prevalence of T. gondii antibodies in overseas animals.......................26
Reported prevalence of T gondii cysts in overseas animal tissue........................28
Dye test results (student nurses and blood donors) .............................................30
Dye test results (nine year old school children)...................................................31
Public hospital discharge records for other acquired toxoplasmosis
manifestations by year, gender and age range .....................................................32
Reported prevalence of Toxoplasma gondii antibodies in pregnant women in
Hamilton ..............................................................................................................33
Seropositivity in blood samples from pregnant women Auckland, n=500..........33
Seropositivity rates overseas in humans ..............................................................35
Seroconversion rates during pregnancy for T. gondii infection...........................38
Percentage of human toxoplasmosis associated with meat types consumed.......39
Summary of information on outbreaks of infection with T. gondii associated with
raw or rare red meat .............................................................................................39
Relative importance of risk factors for an English antenatal population.............43
LIST OF FIGURES
Figure 1:
Figure 2:
Figure 3:
Risk Management Framework...............................................................................3
Diagram of the life cycle of T. gondii....................................................................7
Health outcomes for T. gondii infection ..............................................................16
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
January 2008
SUMMARY
The purpose of a Risk Profile is to provide contextual and background information relevant
to a food/hazard combination so that risk managers can make decisions and, if necessary,
take further action. Risk Profiles include elements of a qualitative risk assessment, as well as
providing information relevant to risk management. Risk profiling may result in a range of
activities e.g. immediate risk management action, a decision to conduct a quantitative risk
assessment, or a programme to gather more data. Risk Profiles also provide information for
ranking of food safety issues.
This Risk Profile concerns Toxoplasma gondii (T. gondii) in red meat and meat products.
The definitive host for T. gondii is the Felidae family i.e. the organism reproduces sexually
only in cats. Most cats in New Zealand have antibodies to T. gondii that indicates exposure
to the parasite at some stage (Thompson, 1999).
It is estimated that approximately one third of humanity has been exposed to T. gondii, and
that 16 – 40% of the UK and USA population has been infected. Higher rates are estimated
in Central and South American and continental Europe.
The reason that toxoplasmosis is not more widely recognised is that the infection is usually
asymptomatic in immunocompetent humans. Clinical symptoms more frequently manifest in
at risk groups with immature and developing immune systems such as the foetus or neonate,
or those with immuno-suppressed or immuno-compromised systems such as organ transplant
recipients, cancer patients and those with HIV/AIDS. Congenital toxoplasmosis may occur if
a previously unexposed pregnant woman becomes infected, with serious outcomes occurring
in a proportion of babies at birth or later in life. Toxoplasmic encephalitis may occur in
AIDS patients.
Toxoplasmosis was a notifiable disease in New Zealand between 1987 and 1996. Hospital
discharge records and notification data during this period do not match and this has been
attributed to under-reporting. Information gathered from discharge records of publicly
funded hospitals in New Zealand between 2000 and 2006 show 84 cases of toxoplasmosis
(non-congenital) and 7 cases of congenital toxoplasmosis, including 3 fatalities. There is very
little information on which to comment on the prevalence of clinical consequences of
toxoplasmosis infection in New Zealand.
The available data on seropositivity of the whole New Zealand population suggest that
infection with Toxoplasma is as prevalent in New Zealand as other developed countries.
Studies of seroconversion in pregnant women in New Zealand suggest a higher prevalence of
congenital toxoplasmosis than has actually been observed.
There are three recognised modes of transmission, direct ingestion of the oocyst originating
from cat faeces contaminating the environment (e.g. soil, water), consumption of the cyst in
animal flesh, and congenital transmission. This Risk Profile addresses the postnatally
acquired form of the disease transmitted through cysts in red meat and meat products. Pig
meat is particularly associated with T. gondii infection.
Risk Profile: Toxoplasma gondii in Red Meat
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Due to the inadvertent nature of infection, it is extremely difficult to ascertain modes of
transmission and, in particular, the extent of infection via the consumption of cysts in red
meat. The United States Department of Agriculture estimate that 50% of T. gondii infections
in that country are related to consumption of raw or undercooked meat, making
toxoplasmosis the third leading cause of deaths caused by infectious foodborne agents in the
USA.
In a survey of consumer meat handling conducted recently by ESR, a question on cooking
preferences for meat found that 1% preferred rare pork, 5% preferred their lamb rare and
19% liked a rare steak. Consumption of raw meat in New Zealand is very infrequent,
according to the survey.
New Zealand has had no reported outbreaks of toxoplasmosis, and there have also been no
case control studies, cohort studies or other risk factor studies. No data could be found on the
prevalence of cysts in red meat or meat products in New Zealand.
While information on seropositivity in New Zealand livestock is limited, it is likely that New
Zealanders domestically produced red meat does contain Toxoplasma. Imported red meat is
less likely to contribute to exposure given that only small amounts of beef and sheep meat are
imported, and pigmeat is required to be frozen. Ameliorating factors for any exposure are
that animal seropositivity appears to overestimate infectivity, and Toxoplasma exposure will
be controlled through cooking and freezing.
Despite the focus on cats as the primary host, ownership of cats as pets has not always been
identified as a risk factor in case-control studies of pregnant women. These studies have
identified the consumption of undercooked meats as a risk factor, although the most recent
study, from England, did not.
The current shortage of information on the prevalence of infection in New Zealand livestock,
or the prevalence of contamination in red meat, precludes a definitive risk assessment of this
food/hazard combination. As noted by the European Food Safety Authority (EFSA),
considerable method development would be required if efficient monitoring programmes for
livestock or food were to be implemented.
Education programmes for vulnerable groups in relation to toxoplasmosis, as recommended
by EFSA, are in place in New Zealand.
Data gaps
•
•
•
•
•
Prevalence of Toxoplasma infection in livestock in New Zealand;
Prevalence of contamination of red meat and red meat products with T. gondii in New
Zealand;
Accurate data concerning toxoplasmosis cases in at risk groups;
Lack of data regarding prevalence of infection in domestic cats (the definitive host) in
New Zealand; and,
Information on awareness by at risk groups in relation to the transmission risks of T.
gondii, this information would be useful in targeting risk communication messages.
Risk Profile: Toxoplasma gondii in Red Meat
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1
INTRODUCTION
The purpose of a Risk Profile is to provide contextual and background information relevant
to a food/hazard combination so that risk managers can make decisions and, if necessary,
take further action. The place of a risk profile in the risk management process is described in
“Food Administration in New Zealand: A Risk Management Framework for Food Safety”
(Ministry of Health/Ministry of Agriculture and Forestry, 2000). Figure 1 outlines the risk
management process.
Figure 1:
Risk Management Framework
Figure reproduced from “Food Administration in New Zealand. A risk management framework for food safety”
(Ministry of Health/Ministry of Agriculture and Forestry, 2000).
In more detail, the four step process is:
1. Risk evaluation
•
•
•
•
•
•
identification of the food safety issue
establishment of a risk profile
ranking of the food safety issue for risk management
establishment of risk assessment policy
commissioning of a risk assessment
consideration of the results of risk assessment
2. Risk management option assessment
Risk Profile: Toxoplasma gondii in Red Meat
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•
•
•
identification of available risk management options
selection of preferred risk management option
final risk management decision
3. Implementation of the risk management decision
4. Monitoring and review.
The Risk Profile informs the overall process, and provides an input into ranking the food
safety issue for risk management. Risk Profiles include elements of a qualitative risk
assessment. However, in most cases a full exposure estimate will not be possible, due to data
gaps, particularly regarding the level of hazard in individual foods. Consequently the risk
characterisation part of a risk assessment will usually rely on surveillance data.
Risk Profiles also provide information relevant to risk management. Based on a Risk Profile,
decisions are made regarding whether to conduct a quantitative risk assessment, or take
action, in the form of gathering more data, or immediate risk management activity.
Toxoplasma gondii was originally chosen as a topic for risk profiling as the significance of
human infections in New Zealand was identified as a knowledge gap in a review conducted
in 1998 (Hasell, 1998). This report is an update of the first Risk Profile on this topic, which
was written in 2002.
The sections in this Risk Profile are organised as much as possible as they would be for a
conventional qualitative risk assessment, as defined by Codex (1999).
Hazard identification, including:
•
•
A description of the organism
A description of the food group
Hazard characterisation, including:
•
•
A description of the adverse health effects caused by the organism.
Dose-response information for the organism in humans, where available.
Exposure assessment, including:
•
•
•
•
Data on the consumption of the food group by New Zealanders.
Data on the occurrence of the hazard in the New Zealand food supply.
Qualitative estimate of exposure to the organism (if possible).
Overseas data relevant to dietary exposure to the organism.
Risk Profile: Toxoplasma gondii in Red Meat
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Risk characterisation:
•
•
Information on the number of cases of adverse health effects resulting from exposure to
the organism with particular reference to the food (based on surveillance data)
Qualitative estimate of risk, including categorisation of the level of risk associated with
the organism in the food (categories are described in Appendix 1).
Risk management information:
•
•
A description of the food industry sector, and relevant food safety controls.
Information about risk management options.
Conclusions and recommendations for further action
Risk Profile: Toxoplasma gondii in Red Meat
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2
HAZARD IDENTIFICATION: THE ORGANISM
The information contained in this Risk Profile is current to the date of publication. Please be
aware that new information on the subject may have arisen since the document was finalised.
The following information is taken from a number of different sources but, unless otherwise
referenced, is primarily derived from a data sheet prepared by ESR under a contract for the
Ministry of Health in 2000-2001. The data sheets are now located on the NZFSA website
and are intended for use by regional public health units. The datasheets will be updated from
time to time, and new versions will be placed on this website:
http://www.nzfsa.govt.nz/science/data-sheets/index.htm
2.1
Toxoplasma gondii
2.1.1
The organism
Toxoplasma gondii is an obligate intracellular protozoan parasite that belongs to the phylum
Apicomplexa, subclass coccidia (Montoya and Liesenfeld, 2004). The organism is classed as
a Category 4 parasite, in that cysts or eggs are shed with faeces of the reservoir definitive
host (in this case members of the cat family), in which the organism is able to reproduce
sexually in large numbers. Excreted organisms are able to infect intermediate hosts such as
warm blooded animals (including humans) and birds. The intermediate hosts are often also
major food sources for humans e.g. livestock providing red meat (Goldsmid et al., 2003).
The organism has a complicated life cycle with numerous stages. The three infectious stages
are tachyzoites, bradyzoites and sporozoites.
The environmentally resistant stage of T. gondii is called the oocyst, which are formed only
in the cat family (Felidae). Cats can become infected and shed oocysts after eating any of the
parasite’s three lifestages (tachyzoite, bradyzoite or sporozoite), often in meat from
intermediate hosts. The time to faecal shedding of oocysts depends on the lifestage ingested,
for example 3 – 10 days for bradyzoites, 21 or more days for tachyzoites or sporozoites. The
ingested bradyzoite appears better adapted to convert into oocysts in the cat’s digestive
system, with nearly 100% of cats shedding oocysts. However, after ingesting tachyzoites and
sporozoites, fewer than 50% shed oocysts.
When mature, the oocysts are discharged into the intestine and passed out with the faeces. At
this stage they are unsporulated and non-infectious. It takes one to five days (atmosphere and
temperature dependent) to sporulate in the environment. Mature oocysts contain two
sporocysts, each sporocyst contains four sporozoites. Sporulation is necessary for the oocyst
to be infective for the next host. The oocyst can remain infective in water or moist soil for
over 12 months (Heymann, 2004). Estimates of the number of oocysts shed after initial
infection ranges from 300,000 to 100 million, thereby logarithmically amplifying the cycle
(Frenkel, 1990). A cat will usually have just one episode of shedding oocysts in its life and
90% of cats that have undergone the intestinal cycle will not shed oocysts again after reinfection with bradyzoites or cysts (Frenkel, 1990). Dubey (1996a) reports, that under
experimental conditions, cats do not shed oocysts after reinoculation with T. gondii tissue
cysts (bradyzoites), but this immunity can wane with time.
Risk Profile: Toxoplasma gondii in Red Meat
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Figure 2 depicts the life cycle of T. gondii from the cat as definitive host and how the
organism is transmitted to humans via contaminated food and water and via undercooked
meat.
Figure 2:
Diagram of the life cycle of T. gondii
Source: Dubey and Beattie, (1988).
The tachyzoite triggers a strong inflammatory response and tissue destruction, manifesting as
clinical symptoms. Under pressure from the immune response, the tachyzoite forms
intracellular cysts or bradyzoites in the tissue. The cyst wall is elastic, thin and can enclose
hundreds of parasites (range 2 - >1000; Dubey, 2001). Sites where the cysts are located can
include visceral organs, such as lungs, liver and kidneys, although muscular and neural tissue
is favoured such as the eye, brain, skeletal and cardiac muscle. Intact, the cysts cause no
harm and the bradyzoites can persist inside for the life of the host. However, if released from
the cysts, bradyzoites transform into tachyzoites, are disseminated to all organs, and restart
the infection (Montoya and Liesenfeld, 2004).
It has been theorised that humans could acquire and ingest oocysts from the fur of an infected
cat. However, even where cats are passing faeces containing thousands of oocysts, none
have been detected on the fur (Dubey, 1995).
2.1.2
Growth and survival
Note: in microbiological terms “D” refers to a 90% (or decimal or 1 log cycle) reduction in
the number of organisms.
Risk Profile: Toxoplasma gondii in Red Meat
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Growth: The organism does not grow in foods or in other environments outside of a suitable
host.
Survival: The oocysts can survive outside of susceptible hosts.
Temperature: Oocysts in faeces or suspended in water retain infectivity for up to 400 days at
temperatures ranging from 4 to 37oC. When frozen at -21oC, unsporulated oocysts (as
excreted into the environment) are killed within 1-7 days at this temperature, but some
sporulated oocysts may survive freezing (Frenkel and Dubey, 1973).
Water Activity: Sporulated oocysts are gradually inactivated by drying. Encysted T. gondii
may survive for 4 days in 8% NaCl.
Bradyzoites are more resistant than tachyzoites to the acidic conditions of the stomach. They
have been shown to survive artificial gastric juice for at least two hours, long enough to
infect humans (Smith, 1993).
2.1.3
Inactivation (CCPs and Hurdles)
T. gondii tissue cysts in meat are inactivated in three ways; cooking, freezing and irradiation.
Temperature: Heating meat throughout to reach a temperature in excess of 66°C is sufficient
to kill cysts in meat (Goldsmid et al., 2003). From a linear regression model, the D times for
cysts (or bradyzoites) in pork were 336 seconds at 49ºC, 44 seconds at 55ºC, 6 seconds at
61ºC and 1 second at 67°C (Dubey et al., 1990). In two of four mutton steaks heated by
microwave to 65ºC, residual infective parasites were detected, possibly due to uneven heating
(Lundén and Uggla, 1992).
Freezing causes cysts in meat tissue to lose infectivity. Various reports have described this
effect at temperatures between –6°C and –40°C (Kotula et al., 1991). These authors also
conducted a more detailed study of the effect of freezing under commercial conditions on T.
gondii tissue cysts in pork. Tissue cysts remained viable for up to 11.2 days at –6.7°C, and
up to 22.4 days at –3.9 and -1°C. However, cysts were rendered noninfective at temperatures
of –9.4°C or less for all time points, except in a very few instances. From the thermal death
curve, a temperature of –12.4°C was obtained as the theoretical temperature at which T.
gondii would be inactivated instantaneously.
In a recent study investigating the effects of time and temperature on the viability of T. gondii
tissue cysts in enhanced pork loins (Hill et al., 2006), meat case temperatures were measured
and were found to vary between -3.2 and +7.0°C. In experimental work related to this,
ingestion of infected enhanced pork loins stored at -5 and 0°C for 7 and 14 days did not result
in infection and shedding of oocysts in seronegative cats. However, pork stored at 3.8 and
6.1°C prior to consumption did give rise to infection. This research suggests that storage of
enhanced pork at or below 0°C is essential to inactivate tissue cysts.
The infectivity of oocysts stored in water at various temperatures has been assessed by mouse
bioassay (Dubey, 1998). Infectivity was destroyed after 1 minute at 60°C or higher, while at
the other extreme, there was no marked loss of infectivity at up to 25°C for 200 days. At 4°C
Risk Profile: Toxoplasma gondii in Red Meat
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infectivity to mice remained after 54 months. Smith (1992) reports that treatment with
boiling water for five minutes is effective in destroying oocysts.
Preservatives: The organism has been demonstrated to be rendered noninfective by curing in
sodium chloride and sucrose (approximately 15% of each by weight of meat) at 4°C for 64
hours (Lundén and Uggla, 1992). However, cured pork was cited as a risk factor for
infection in a case control study in Italy (Buffolano et al., 1996). The authors commented
that meats are sometimes cured using much lower levels of salt or sucrose.
Meat enhancement solutions (sodium chloride plus potassium/sodium lactate): Hill et al.
(2004) reported data on the viability of T. gondii tissue cysts in pork loins treated with
enhancement solutions. This study found that 2% sodium chloride or ≥1.4% potassium or
sodium lactate, used alone or in combination with other components, was able to prevent the
subsequent development of infection in cats fed infected pork loins stored for up to 45 days at
4°C.
Subsequent research by Hill et al. (2006) investigated how quickly the successful
enhancement solutions used in their previous study were able to inactivate T. gondii tissue
cysts in pork loins. Storage of pork loins at 4°C for 8 hours post-enhancement prior to
consumption was found to be sufficient time for inactivation to occur.
Radiation: Exposure of tachyzoites to 70 J m-2 ultraviolet light renders the organism noninfectious.
A minimal effective dose (MED) of Co60 at 0.6kGy was calculated to inactivate cyst
infectivity (Song et al., 1993). Dubey and Thayer (1994) found a lower dose of 0.4kGy was
sufficient and that temperature during irradiation had no marked effect. Because of the
variability in the number of cysts present in pork and variation in carcass sizes, a 1 kGy dose
is recommended for complete disinfection (Smith, 1992).
Pressure: High pressure processing (HHP) of ground pork containing viable T. gondii cysts
was studied at various pressure and time combinations (Lindsay et al., 2006). Results of
mouse bioassay found that none of the cysts exposed to 300 or 400 Mpa remained infective;
while cysts processed at 200, 100 or no pressure (control) remained infective regardless of
treatment time.
2.1.4
Sources
Human: There have been no reports of direct person-to-person spread nor transmission
during breastfeeding. Transplacental transmission from mother to baby can occur if the
mother is infected for the first time during, or just before, pregnancy (Montoya and
Liesenfeld, 2004). Transmission by organ transplantation can also occur. A large number of
blood donors are potentially seropositive, however cases of transfusion-transmitted
toxoplasmosis have only been reported in acute leukaemia cases undergoing chemotherapy
(Smith, 1997).
The sub-clinical human infection can be chronic and become activated if the immune system
becomes weakened.
Risk Profile: Toxoplasma gondii in Red Meat
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Animal: Cats are the definitive host and warm-blooded mammals and birds are intermediate
hosts. Contamination of the environment by oocysts shed in faeces by cats is a possible route
of transmission. Although the risk from handling cat litter has been proposed, ownership of a
cat has not been found to be a risk factor in several studies (AFSSA, 2005).
Transmission directly through contact with intermediate host animals does not appear to be
important in the epidemiology of human infections.
Animals such as flies, earth worms and cockroaches that have come into contact with
infected faeces may harbour the organism and mechanically spread the oocysts (Dubey,
1996a).
Food: Along with poor hand hygiene, the consumption of poorly cooked meat and badly
washed raw vegetables are the principal food related risk factors for human infection
(AFSSA, 2005). Especially important are vegetables originating from gardens where there
may be cats (Smith, 1993).
Meat from bovines is less frequently contaminated by cysts than pig, sheep and goat meats.
Unpasteurised goat’s milk has also been implicated in some outbreaks (Smith, 1993; Sacks et
al., 1982; Skinner et al., 1990). Meat from birds, including poultry, may contain T. gondii
cysts (AFSSA, 2005). Other meats that may contain cysts are rabbit, horse, and game (e.g.
deer), and occasionally, cured meats (ham).
Environment: Consumption of water contaminated by oocysts shed by cats can result in
infection, and several outbreaks have been linked to drinking insufficiently treated water.
Oocysts can survive in soil for several months (Frenkel, 1990). Soils may be important
intermediates in the transmission from cats to humans via buried faeces.
Transmission Routes: There are five transmission routes identified (Leroy, 2005).
i) The ingestion of raw or inadequately cooked infected meat, or ingestion of uncooked foods
that have been in contact with such meat
ii) Ingestion from oocysts through direct contact with faeces passed by an infected cat or
indirect contact such as contaminated soil such as when gardening, or eating unwashed
vegetables, or drinking water that has been in contact with contaminated cat faeces.
iii) Transplacental infection during a primary infection of the mother.
iv) Organ transplantation or blood transmission (seropositive donor to seronegative
recipient).
v) Accidental inoculation by laboratory personnel, for example, the use of contaminated
needles or work with infected animals.
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3
HAZARD IDENTIFICATION: THE FOOD
3.1
Relevant Characteristics of the Food: Red Meat and Meat Products
As the organism does not grow outside a live host, the characteristics of the food group are
less relevant in terms of contributing to risk. Specific edible meats found to contain cysts
include (Smith, 1991):
•
•
•
•
•
•
•
Beef and veal;
Small game animals (including rabbits);
Fowl (chicken and pigeons);
Horse meat;
Deer and elk (wapiti) meat;
Mutton, lamb and goat meat; and
Pork.
Cysts have also been reported in wallabies (MAF, 1974; 1980; 2000), little blue penguins
(Mason et al., 1991), and possums (Eymann et al., 2006), although these animals are not
considered livestock.
Beef and veal are generally considered as less likely to be contaminated; clinical disease is
rare in cattle and the organism is rapidly eliminated from tissues (Smith, 1991).
The meats listed above all fall into the risk profile category of red meat, apart from chicken
and pigeons. While raw meats have been most commonly implicated in cases of
toxoplasmosis, cured meats such as ham have also been shown to occasionally contain cysts
(Warnekulasuriya et al., 1998).
Although visual examination or serological testing can be used in the field or slaughterhouses
to prevent other parasites (Taenia solium and Trichinella spiralis) from entering the food
supply, these are not options for T. gondii due to the length of time and complexity of the
extraction procedures and assays (Gamble, 1997). Consequently control mechanisms must
focus on destruction of cysts via cooking or other mechanisms.
The effect of heating and freezing on inactivation of T. gondii cysts has been reviewed in
Section 2.1.3.
Freezing to -12.4°C has been suggested as the theoretical temperature for instant inactivation
of T. gondii cysts in meat tissue (Kotula et al., 1991). In New Zealand, meat cuts presented
for retail sale (butchers, supermarkets) will not usually have been frozen. However,
wholesale meat used in the production of sausages, meat pies, etc. is likely to have undergone
freezing at some stage (Graeme Keeley, Technical Manager, PPCS, personal
communication). Only a small proportion of meat for domestic consumption will have been
frozen prior to sale (Clyde Daly, AgResearch, personal communication). The current chilling
regime used for “Quality Mark” meat production requires a temperature of 7°C or less prior
to shipping, with 4°C achieved by retail sale. This means that if the cysts are present in the
meat at slaughter, they may still be present in retail chilled meats.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
11
January 2008
3.2
The Food Supply in New Zealand
There are 17,000 commercial sheep and beef cattle farms in New Zealand, most of which are
owned and operated by farming families. Livestock numbers for New Zealand in 2005 are
shown in Table 1. A high proportion of sheep and beef production is exported.
Table 1:
Livestock numbers, production and export for New Zealand
Livestock type
Number of animals (000 head)
For year 2005
Meat production in year to
September 2005 (000 tonnes
carcass weight)
Sheep
39,928
Beef
4,431
Pigs
Deer
Goats
389
1,705
142
105 mutton
438 lamb
23 veal
629 beef
50
N/a
N/a
N/a: Not available
Source: MAF sonzaf website accessed 17.07.07 MAF (2007)
One major technological advancement has been the extension of shelf life for chilled meat,
which means that each year a greater proportion of meat is being exported as chilled cuts
rather than frozen carcasses. In 2006, 15% of all lamb exports were exported chilled (MIA,
2006).
As the figures indicate, the vast majority of meat production in New Zealand is exported.
New Zealand has a relatively small pork industry, which focuses on the domestic market.
Since 1995, pigmeat production has been relatively static averaging 49,000 tonnes per year,
although it appears that pigmeat consumption has been slowly increasing (New Zealand Pork
Industry Board, 2001).
3.2.1
Imported food
Approximately 4,500 tonnes of meat preparations were imported during the year to
September 2005, with almost 80% coming from Australia.
New Zealand imports relatively small amounts of beef and sheep meat according to data from
Statistics New Zealand. For the year to September 2005 approximately 3,200 tonnes of beef
carcasses and cuts and 3,100 tonnes of sheepmeat (all types) were imported from Australia.
Imports of pork have increased steadily to now make up approximately 38% of total supply
(31,864 tonnes in 2005), mostly sourced from Australia and Canada. New Zealand maintains
Risk Profile: Toxoplasma gondii in Red Meat
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January 2008
an Import Health Standard for the importation of pork, including a requirement that the pork
is frozen to –18°C (Anon, 2006). This means that in theory imported pork should be T.
gondii free; see http://www.pork.co.nz/profile.asp). Currently due to Import Health
requirements, Canadian pigmeat is imported uncooked, held in transitional facilities, cooked
and then released onto the New Zealand market so is unlikely to harbour T. gondi.
These data, when compared to the production and export figures above, suggest that
approximately 5% of New Zealand’s beef and sheep meat for domestic consumption derives
from Australia, while approximately 38% of pigmeat for domestic consumption is imported,
principally from Australia and Canada.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
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4
HAZARD CHARACTERISATION: ADVERSE HEALTH EFFECTS
When T. gondii oocysts/tissue cysts are ingested by humans or other animals, digestive juices
break down the cyst to release the bradyzoites, which transform to tachyzoites in the small
intestine and cause infection. The organism then penetrates the intestinal wall and migrates
throughout the body where it can invade a variety of tissues (a vacuole around the organism
protects against the host’s defence mechanism). Within the tissues, the parasite multiplies
asexually, forming tissue cysts (Murrell, 1995; Hill and Dubey, 2003; Montoya and
Liesenfeld, 2004).
4.1
Symptoms
Incubation: A foodborne outbreak in Australia reported an incubation period of 3 – 25 days,
with a mean of 11 days (Robson et al., 1995). In another outbreak associated with cats
(oocysts), the incubation period was 5 – 20 days (Heymann, 2004).
Symptoms: In immunocompetent humans, the infection is common although under-reported
because 80-90% of infections are asymptomatic. Clinical toxoplasmosis is rare. In about 1020% of cases, a viral-like febrile illness occurs with lymphadenopathy (swollen lymph nodes)
(Mead et al., 1999). This is usually mild and self-limiting and individuals seldom seek
medical attention (Smith, 1997).
Clinical toxoplasmosis typically affects individuals with developing or impaired immune
systems such as the developing foetus, the elderly, medically immunosuppressed patients,
and those who are immunocompromised by disease (e.g. AIDS) (Smith, 1997). The central
nervous system is the site most typically affected by infection, with a wide variety of
symptoms (Montoya and Liesenfeld, 2004).
It has been reported that pregnant women are significantly (2.2 times) at higher risk of
seroconversion for toxoplasmosis than non-pregnant women (7.7 times higher if the woman
is an adolescent) (Avelino et al., 2003). This has been ascribed to alterations in the immune
system necessary for the tolerance of the foetus and/or hormonal imbalances (Daunter, 1992).
If a previously unexposed pregnant woman becomes infected, the parasite can be transmitted
across the placenta to cause congenital toxoplasmosis, the most commonly cited health
concern. The mother may remain asymptomatic (Goldsmid et al., 2003). In general, the
older the mother, the more likely they are to be seropositive which means that those entering
motherhood early may have more risk of initial infection while carrying their child. Women
who are seropositive for T. gondii prior to pregnancy, but who are healthy and
immunocompetent, do not transmit the parasite to their foetuses.
Transplacental infection occurs when rapidly dividing tachyzoite cells circulate in the
bloodstream and cross the placenta to infect the foetus (Heymann, 2004). While the infection
may not damage the foetus, it is capable of causing death or serious neurological damage in
up to 5% of infections (Gilbert et al., 2006). Hydrocephalus, intracranial calcification and
retinochoroiditis are the most common manifestations of tissue damage due to congenital
toxoplasmosis (Gras et al., 2001).
The probability of transmitting the parasite increases with the trimester of pregnancy; rates of
Risk Profile: Toxoplasma gondii in Red Meat
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January 2008
transmission are more than 60% in the last trimester. However, frequency of transmission
and severity of disease are inversely related (Montoya and Liesenfeld, 2004). Three to four
percent of infected neonates die, while the remainder will suffer from various forms of long
term disease (mental retardation, blindness and epilepsy) (Smith, 1997). It has been estimated
that in congenital infections of babies, 8-10% have brain and eye lesions while 10-13%
become visually impaired. Nearly all those born with subclinical disease will develop
symptoms later on.
Although the immune systems of elderly people (>65 years) undergo changes that should
make them more susceptible to toxoplasmosis, there is no evidence that the parasite becomes
reactivated in healthy seropositive elderly individuals (Smith, 1997).
In immuno-compromised people (those suffering from AIDS or undergoing
immunosuppressive therapy) disease seems to result from the activation of a previously
subclinical infection. Reactivation most often involves the central nervous system and
symptoms can include meningoencephalitis, maculopapular rash, generalised skeletal muscle
involvement, cerebritis, chorioretinitis, pneumonia and myocarditis (Heymann, 2004). It has
been estimated that up to 30% of AIDS patients in Europe and 10% in the USA will die from
toxoplasmosis, the majority via toxoplasmic encephalitis (Luft and Remington, 1992).
Although any organ may be involved, infection of the brain is that most often reported, a
persistent severe and bilateral headache progressing to confusion, lethargy, ataxia and coma.
The predominant lesion is necrotised tissue in the thalamus (Renold et al., 1992).
Condition: Toxoplasmosis.
Toxins: T. gondii does not produce a toxin.
Long Term Effects: In healthy people infection rarely leads to death. Vulnerable populations
are most likely to experience long term effects after infection. Examples include visual
impairment and brain damage. The role of toxoplasmosis in inducing Guillain-Barré
syndrome is probably infrequent (Smith, 1993).
Treatment: Currently there is no human vaccine for the disease. Treatment is not routinely
administered for a healthy immunocompetent host. In immuno-compromised patients such
as patients with symptomatic toxoplasmosis, prophylactic treatment with pyrimethamine
can be given in combination with sulfadiazine and folinic acid (to avoid bone marrow
depression). Clindamycin has been additionally used to treat ocular toxoplasmosis
(Heymann, 2004). However these drugs can be problematic when used with pregnant
women. Spiramycin is commonly used to prevent placental infection (Heymann, 2004).
The potential health outcomes are summarised in Figure 3.
Risk Profile: Toxoplasma gondii in Red Meat
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Figure 3:
Health outcomes for T. gondii infection
Primary infection
Children and adults
During pregnancy or
shortly before conception
90% asymptomatic
10% lymphadenitis,
chorioretinitis, rarely
myocarditis or myositis
Placenta
latent infection
(asymptomatic)
Potential for transplacental
transmission and congenital
infection
Reactivation in immunocomprised
hosts (patients with AIDS, organ
transplantation, cancer, or taking
immunosuppressants)
Toxoplasmic encephalitis
Source: Montoya and Liesenfeld, 2004
Risk Profile: Toxoplasma gondii in Red Meat
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4.2
Types Causing Disease
T. gondii has a low genetic diversity with only three genetic types I, II and III classified on
the basis of antigens, isoenzymes, and restriction fragment length polymorphism (Hill and
Dubey, 2003). Most strains isolated from patients with AIDS are Type II. Type I and II
strains have been recorded in patients with congenital disease, whereas strains isolated from
animals are mostly Type III (Montoya and Liesenfeld, 2004; Howe and Sibley, 1995;
Nowakowska et al., 2006).
The differential occurrence of these types is not absolute however. For example, studies of T.
gondii isolates from free range asymptomatic chickens in various South American countries
have found all three genetic types (Dubey et al., 2002b; Dubey et al., 2006).
4.3
Dose Response
No information has been found regarding the dose response relationship for Toxoplasma
gondii in humans. For ethical reasons, establishing a dose infection relationship based on
experimental trials and healthy human volunteers is not foreseeable. In animal studies, the
feeding of graded doses of oocysts to pigs (an intermediate host) found that one sporulated
oocyst was infective, the results were 13/14 pigs fed 10 oocysts, 13/14 pigs fed 1 oocyst and
4/14 pigs fed < 1 oocyst were infected. Higher isolations were observed in the tongue as
opposed to the brain and heart (Dubey et al., 1996). In another study, ten bradyzoites were
not infective to cats, but higher numbers (100 and 1000) caused shedding of infective oocysts
(Dubey, 1996b; Dubey, 2001).
4.4
High Risk Groups in the New Zealand Population
The following sections provide information on groups in the New Zealand population for
whom infection by Toxoplasma could have serious consequences.
4.4.1
Pregnant women
Live births data for the year to September 2007 were 62,360 (http://www.stats.govt.nz/
accessed January 2008).
4.4.2
Immune compromised
HIV: In 2005, 218 people in New Zealand were newly diagnosed with HIV, the highest since
records began in 1985. Since 1985, a total of 2474 cases of HIV have been recorded in New
Zealand (ESR, 2006).
AIDS: There were 49 notifications of AIDS cases in 2005 and 8 deaths. Since 1983, there
have been 891 AIDS notifications in New Zealand. The number of deaths due to AIDS
peaked at 66 in 1992. In the last four years, there have been approximately 10 deaths each
year (ESR, 2006).
Risk Profile: Toxoplasma gondii in Red Meat
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Cancer: The most recently available statistics on the incidence of cancer and cancer mortality
in
New
Zealand
are
from
2002
(website
accessed
15.08.06
http://www.nzhis.govt.nz/stats/tables/cancer2002.xls and publications/cancer.html).
In that year, 17,943 new cases of cancer were registered, made up of 9,399 (52.4%) males
(348.2 cases per 100,000) and 8,544 (47.6%) females (287.0 cases per 100,000). During the
same period, mortality due to cancer was 7,800 (120.9 cases per 100,000) made up of 4125
males (142.8 per 100,000) and 3675 females (104.9 per 100,000). It is uncertain what
proportion of the New Zealand population is suffering from cancer at any particular time.
Recipients of organ or tissue donations: The New Zealand Organ Donation website gives the
following numbers for transplants performed in 2005; kidney (deceased donor) 47; kidney
(living donor) 46, liver (deceased donor) 24, liver (living donor) 4, heart 13, lungs 8,
pancreas 2 (http://www.donor.co.nz accessed October 2006). It appears likely that the total
New Zealand population of surviving major organ transplant recipients is less than 2000
people (0.05% of the total population).
Risk Profile: Toxoplasma gondii in Red Meat
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5
EXPOSURE ASSESSMENT
5.1
The Hazard in the New Zealand Food Supply
5.1.1
Test methods
Most of the information regarding the prevalence of Toxoplasma gondii is derived from
studies that measure antibodies against the organism present in the blood of humans and
animals. A review carried out by Remington et al., (1995) has examined the range of
antibody detection methods including the Sabin-Feldman dye test, indirect fluorescent
antibody test (IFAT), complement fixation test (CFT), the modified agglutination test (MAT)
and enzyme-linked immunosorbent assay (ELISA).
To detect Toxoplasma in meat or tissue samples, extracts are used in mouse-based assays to
demonstrate infectivity. The mice are inoculated orally or subcutaneously with the extracts,
and then the mouse sera can be examined for antibodies, and/or tissues can be examined
microscopically. Assays have also been used with cats and, because of the large numbers of
oocysts they shed following infection, they are more sensitive than mice for detecting
infective cysts (Dubey, 2001). However, the mouse bioassay is more commonly used.
Results from such mouse assays have not consistently demonstrated that material extracted
from the tissue of seropositive animals is infective. In a Canadian study, although
seroprevalence of Toxoplasma antibodies in pigs was between 3.5 and 13.2%, none of the
extracts tested showed any infectivity in the mouse bioassay (Gajadhar et al., 1998). This
suggests that serological data from mouse assays may not accurately assess the risk from
improperly cooked pork products.
Direct detection in foods is difficult, one reason being that the methodology requires the
concentration of the organism from muscle tissue prior to detection. Due to the low numbers
of oocysts present in environmental samples (e.g. water), detection methods are largely based
on filtration similar to those used for other parasites (Fayer et al., 2001).
The presence of Toxoplasma DNA in samples (including commercial meats) has more
recently been demonstrated using the polymerase chain reaction (PCR) (Aspinall et al.,
2002). PCR detects the presence of T. gondii DNA but not necessarily the presence of viable
cysts.
5.1.2
Toxoplasma prevalence in livestock animals in New Zealand
There are no data on the prevalence of Toxoplasma in red meat in New Zealand. Some
reports provide indirect data on the prevalence of infection in livestock and other animals,
including pets (see Section 7.3.1).
Pigs: A review of parasites of New Zealand pigs stated that the prevalence of Toxoplasma in
New Zealand pigs is unknown, although there have been occasional reports of clinical
toxoplasmosis in farmed pigs (Fairley, 1996).
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Sheep: The “Veterinary Handbook” prepared for the New Zealand Veterinary Association
states that the incidence of toxoplasmosis in young ewes is “up to 30% with placentitis and
abortion or perinatal deaths. Up to 90% of ewes may have serum antibodies by 2 years.
Disease rare in other species.” (Manktelow, 1984). Reports in Surveillance (MAF, 2001;
2002) stated that most sheep abortions in New Zealand are caused by T. gondii infection or
Campylobacter fetus. Infection with T. gondii was noticeably more prevalent as the lambing
season approached.
A live Toxoplasma vaccine for sheep has been developed by AgVax at Wallaceville and is
registered and in use in New Zealand. The vaccine uses the s48 strain of the tachyzoites
which have lost their lifecycle persistence. After vaccination, the s48 tachyzoites multiply in
the young sheep for approximately seven days. Bradyzoites and subsequent tissue cysts do
not develop and the parasite dies, leaving the sheep immune and in the long term, the meat is
safe to consume. The vaccine is a preventive measure in order to reduce the risk of abortion
caused by Toxoplasma infection during subsequent pregnancy (Murray Wilkins, AgVax,
personal communication). More information on the vaccine can be found at the following
website address;
http://www.agvax.com/animal_health/sheep/toxovax/technical_manual/toxoplasmosis_the_in
fection.htm. The vaccine is most commonly used for the vaccination of ewe hoggets or rising
two-tooth ewes joining the flock.
In 2004, 61 abortions in sheep due to T. gondii were reported (MAF Biosecurity Authority,
2005).
Goats: Thompson (2001) reported T. gondii as the most common cause of infectious abortion
in goats although the author notes that caprine abortions associated with Neospora and
Sacrocystis species could be easily misdiagnosed as toxoplasmosis. Opel et al. (1991)
reported on the seropositivity of New Zealand domesticated clinically normal goats from 17
farms. Positive samples were found from the sera of 7% of kids (n=88), 23% of yearlings
(n=65) and 37% of adults (n=145). This increase of positive titres with age was statistically
significant, as was a higher frequency of positives in dairy compared to fibre breeds. There
were no data on feral goats, although the author proposed that the infection rate in dairy goats
could reflect intensive husbandry practices. In addition, hay feed might be contaminated by
cats, which implies greater prevalence in domesticated rather than feral populations.
Cattle: A review of infectious diseases in cattle in New Zealand stated that infection with T.
gondii is probably common in New Zealand but the clinical disease is rarely recorded
(Vermunt and Parkinson, 2000).
Deer: The prevalence of T. gondii infection in feral deer is not known. In 1997, MAF
assembled a farmed deer serum bank of 1,150 specimens, of which a random sub-sample of
417 were tested for toxoplasmosis antibodies. The overall seroprevalence was 219/417
(52.5%) (using reciprocal titres of ≥ 8 as positive). Seroprevalence increased with age from
15.4% in < 1 year-olds to 86.6% in deer 8 years old and above. The prevalence is consistent
with overseas deer surveys (Reichel et al., 1999).
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5.2
Food Consumption: Red Meat and Meat Products
Red meat consumption has declined over the last 20 years, mainly due to mutton and lamb,
see Table 2. A major shift in consumption patterns has taken place with major and smaller
gains by the poultry and pork industries respectively.
Table 2:
New Zealand domestic meat consumption per capita 1985, 1995, 1996,
1999 to 2006 (kg/person/year)
Year
1985
1995
1996
1999
20011
2001/022
(Sept. end)
2002/033
(March end)
20054 (June end)
Mutton
and Lamb
27.3
23.2
20.6
14.3
16.6
16.1
Beef and
Veal
36.5
34.6
37.8
31.2
27.1
27.6
Pig meat
Poultry
14.2
15.7
16.1
17.1
16.5
17.3
Total Red
meat
78.0
73.5
74.5
62.6
60.2
61.0
15.0
26.2
25.1
26.8
31.0
34.1
Total
Meat
93.0
100.1
99.8
89.5
91.3
95.1
15.3
29.4
17.9
62.6
35.9
98.5
13.6
32.4
19.6
65.6
37.1
102.7
From New Zealand Meat and Wool Board's Economic Service (MWBES) Annual Review of the Sheep and
Beef Industry, 1999-2000.
1
Data from website; http://www.beef.org.nz/statistics/slides.asp
2
Compendium of New Zealand Farm production statistics, April 2003.
3
PIANZ, December 2003
4
New Zealand Meat and Wool Board's Economic Service (MWBES) Meat Consumption and Expenditure June
Qtr 2006
The meat consumption figures for New Zealand in Table 2 are similar to estimates made for
the Australian population (Baghurst, 1999). An international comparison of meat
consumption as calculated for 2003 is given in Table 3.
Table 3:
International comparison of meat consumption, 2003 (kg/person/year)
Bovine meat
Country
Argentina
Australia
Canada
New Zealand
UK
USA
54.7
45.1
34.3
26.4
20.9
41.9
Sheep and goat
meat
1.5
14.4
1.0
24.8
5.9
0.5
Pigmeat
Poultry meat
5.1
21.1
27.4
20.7
26.0
30.1
19.4
35.6
36.3
35.2
30.0
50.2
Source: http://faostat.fao.org/
The figures given in Table 2 represent the meat available for consumption in New Zealand.
Information on amounts of meat reported to be actually consumed by individuals can be
Risk Profile: Toxoplasma gondii in Red Meat
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21
January 2008
abstracted from the 1997 National Nutrition Survey (NNS) (Russell et al., 1999). FSANZ
have carried out an analysis of this dataset (ANZFA, 2001), including application of a set of
standard recipes, to allow composite foods to be reduced to their component parts. Table 4
gives the estimates for New Zealand domestic meat consumption derived by ANZFA and
compares those levels of consumption to the estimates based on meat available for
consumption in Table 2.
Table 4:
Meat type
unit
Beef and veal
Sheep and
Lamb
Pig meat
Deer meat
Total red
meat
Mean estimates of New Zealand domestic meat consumption in 1997 and
estimates of meat available for consumption, 2004
Estimated
consumption
(1997)*
g/person over 15
yrs/day
87.9
13.7
Amount available for consumption (2004)#
kg per person per
year
29.93
23.54
g per person per day
7.86
3.28
64.6kg
21.5
8.8
181g
32.3
0.9
134.9g
82.0
64.5
*
from ANZFA analysis of 1997 National Nutrition Survey data (ANZFA, 2001)
#
recalculated from Table 2 and 2003 import data, (population at June 2004; 4,009,200) source:
http://www.stats.govt.nz/
The difference between these two estimates of consumption will reflect wastage (meat
available for consumption, but not consumed) and under-reporting in the National Nutrition
Survey (NNS). Through use of standard recipes the FSANZ analysis of the most up to date
(1997) NNS data will include all meat consumed, including meat that is consumed as a
component of a processed food such as meat pies or luncheon meat (ANZFA, 2001).
The analysis of the 1997 NNS data concluded that 77.7% of the population consumed red
meat (cattle, sheep or pig meat) during any 24 hour period. The mean daily consumption was
172.5 g. The median daily consumption, for consumers only, was 124.1 g/day. The 97.5th
percentile daily consumption, for consumers only, was 616 g/day.
Table 5 represents an analysis of dietary records from the 1997 National Nutrition Survey
and shows a breakdown of total red meat and red meat product consumption on the basis of
number of servings and on the basis of consumption weight. Beef is the predominant red
meat consumed in New Zealand with over 50% of the total red meat consumed by weight.
Pig meat contributes around 15% and sheep meat approximately 9%.
Risk Profile: Toxoplasma gondii in Red Meat
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January 2008
Table 5:
Types of red meat and meat products consumed, by servings and by
weight
Meat type
Percentage of total red Percentage of total red
meat consumed
meat consumed
(by servings)
(by weight)
Beef (including veal)
Corned beef
Beef mince and beef mince recipes
(patties, hamburgers, etc)
Beef cuts (steak, roast, schnitzel, etc)
Sheep meat (Lamb, hoggett and mutton)
Hoggett/mutton cuts
Lamb cuts
Lamb mince and lamb mince recipes
Pig meat (including ham and bacon)
Pig meat cuts
Pig meat mince
Bacon
Ham
Mixed meat products
Sausages, saveloys, frankfurters and
hotdogs
Other meats
Venison
Other
5.3
6.3
14.7
5.0
24.1
20.2
26.2
4.1
6.0
0.1
3.6
5.2
0.1
6.8
0.1
7.3
11.5
8.3
0.1
2.9
4.3
13.6
15.1
0.4
8.9
0.5
4.6
Qualitative Estimate of Exposure
It is not possible to make a qualitative estimate of exposure to T. gondii from red meat in
New Zealand. Although there is some evidence to suggest that a proportion of the farmed
animals in New Zealand have been infected with the organism, it is not possible to translate
this seropositivity information into data regarding infectiveness. While estimates for the
number of servings of red meat consumed and the median serving size can be made, there is
insufficient information to estimate the frequency of contamination or the likely level of
contamination at retail.
In addition, the infectivity of any Toxoplasma in imported pork is likely to be low, given the
requirement for freezing at -18˚C, which should destroy the organism.
5.3.1
Number of servings and serving size
The estimation of total number of servings of red meat consumed on a per annum basis
involves a number of assumptions:
• That the sample set employed for the NNS is typical of the total population;
• That the results of the 24 hour dietary recalls are typical of the full 365 day period of one
year; and,
Risk Profile: Toxoplasma gondii in Red Meat
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January 2008
• That the consumption of red meat by the population less than 15 years of age will not be
significantly different to that for the survey population (the NNS only surveyed people 15
years and older).
Analysis of dietary records from the 4636 people interviewed for the 24 hour dietary recall
survey carried out as part of the 1997 NNS (Russell et al., 1999) identified approximately
5,800 records of food items consumed (servings) which were likely to have contained red
meat, red meat products, ready-to-eat (RTE) red meat products or red meat extracts. On this
basis red meat and red meat products should be considered to be a very commonly consumed
group of foods, with only milk (dairy products) and cereal grains being consumed with
similar frequency.
T. gondii principally constitutes a risk to the foetus due to consumption by the mother leading
to in utero exposure. To assess the number of servings of red meat for the New Zealand
population which may result in foetal exposure, the number of servings for the total
population may be multiplied by the annual live births rate (for New Zealand; 58,250 to June
2006 calender year) as a percentage of the June 2006 total estimated population (4,140,300)
gives a birth rate of 14.1 per 1,000 per annum. Identical to the USA rate of 14.1 births per
1,000 in 2003, (see website http://mchb.hrsa.gov/whusa_05/pages/0425lb.htm accessed 24
August 2006).
For the population as a whole, due to the large number of foods which may contain red meat
as a minor component (e.g. meat-based soups) serving sizes will vary over a very wide range.
The FSANZ analysis of the 1997 NNS data (ANZFA, 2001), which includes the use of
standard recipes to reduce composite foods to their component parts, calculated a median
total daily meat intake for consumers of 124.1 g/day. Based on the estimate of 5,800 servings
from the survey and 3,599 (of 4636 people surveyed) consumers, it can be calculated that, on
average, this median intake will represent 1.6 servings of red meat. This calculation gives a
median serving size of 77.6 g, a mean serving size of 107.8 g and a 97.5th percentile serving
size of 385 g.
5.3.2
Frequency of contamination
No information is available on the frequency of contamination of red meat and red meat
products with T. gondii in New Zealand.
5.3.3
Predicted contamination level at retail
No information is available on which to base a prediction of contamination of red meat and
red meat products at retail with T. gondii.
5.3.4
Growth rate during storage and most likely storage time
The organism does not grow in foods or in other environments outside of a suitable host.
T. gondii is destroyed by freezing at temperatures of –12.5°C or lower. Discussion with meat
industry representatives suggest that meat reaching the consumer as meat cuts is unlikely to
have been frozen, while processed meat products (e.g. sausages) are highly likely to have
been manufactured from frozen meat. Approximately 60% of the 5800 servings identified
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
24
January 2008
from the 1997 National Nutrition Survey as being likely to contain red meat would be
classified as manufactured meat products. It is likely that all of these servings would have
undergone a sufficiently rigorous freezing regime to destroy the organism.
5.3.5
Heat treatment
T. gondii is susceptible to heat inactivation, and this occurs within a few seconds at
temperatures above 60°C (see section 2.1.3). Red meat servings cooked medium to well
done are unlikely to contain active organisms. Thomson and Lake (1995) carried out a
survey of meat consumption and cooking practices amongst 902 respondents in the Hawke’s
Bay and Christchurch. Approximately four percent of respondents reported consuming
servings of meat that were cooked to a ‘rare’ condition.
In a recent ESR postal survey of meat handling in the home (Gilbert et al., 2005), 1000
randomly chosen people across New Zealand were asked their preferences when cooking
meat and poultry. Approximately one third replied to the survey. Table 6 below displays the
results.
Table 6:
Data for meat and poultry cooking preferences in New Zealand
Meat type
Roast lamb
Roast pork
Steak (pan fried)
Chicken (roast)
Sausages (pan fried)
Minced
beef/hamburgers
Chicken livers
Raw (%) Rare
(%)
0
16 (5)
0
2 (1)
2 (1) 58 (19)
0
0
0
0
Medium Well done
(%)
(%)
130 (43) 138 (46)
53 (19)
191 (67)
152 (50)
78 (26)
35 (27)
48 (38)
40 (14)
217 (75)
Very well Total* Don't
done (%)
eat
16 (5)
300
17
38 (13)
284
32
13 (4)
303
11
45 (35)
128
8
31 (11)
288
27
0
0
53 (18)
209 (70)
35 (12)
297
18
0
1 (1)
17 (22)
41 (53)
18 (23)
77
219
* the total column of respondents does not include the “don’t eat” column therefore only those expressing a
preference are used in percentage calculations.
As expected, pan-fried steak was the meat that people were most likely to prefer rare or raw.
5.3.6
Exposure summary
While red meat and meat products constitute a very commonly consumed food, the lack of
any data on the prevalence of the organism in foods hampers any attempt to assess likely
exposure. The organism if present in red meat is likely to face either one of two significant
hurdles: freezing for processed meat products or cooking for fresh meat cuts.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
25
January 2008
5.4
Overseas Context
5.4.1
Seroprevalence in animals
The prevalence of antibodies for Toxoplasma in animals overseas derived from serological
tests has been summarised in Table 7.
Table 7:
Country
Australia
(Tasmania)
Australia
Australia
Brazil
Canada
France
Iran
Mexico
Norway
Serbia
Spain (Grand
Canary Island)
USA
Reported prevalence of T. gondii antibodies in overseas animals
Number
tested
160
145
173
114
30
139
1,159
Animal tested
Percentage
seropositive
16.9
61.7
2.3
0
22.3
7.2
7.4-9.2
Lambs
Other sheep
Vealers
Other cattle
Cracker pigs
Other pigs
Sheep
151
85
439
240
194
104
2,800
Tasmanian pademelons
Bennett’s Wallabies
Goats
Sheep
Cattle
Water buffaloes
Pigs
3.3
17.7
28.9
18.7
1.0
3.8
8.6
164
93
290
400
588
490
1203
707
Lambs
Ewes
Cattle
Goats
Sheep
Cattle
Pigs
Goats
22.0
65.6
0
30
35
11.9
8.9
3.2
NS
Sheep
18.0
NS
Cattle
5.1
NS
Pigs
2.5
611
511
605
1052
Cattle
Ewes
Pigs
Goats
76.3
84.5
28.9
63.3
3,707
Pigs
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
32 (range <1
26
Reference
Munday, 1975
Munday, 1975
Munday, 1975
Munday, 1975
Munday, 1975
Munday, 1975
O’Donoghue et al.,
1987
Johnson et al., 1988
Johnson et al., 1988
Pita Gondim et al.,
1999
Gajadhar et al.,
1998
Dumètre et al., 2006
Sharif et al., 2006
Garcia-Vazquez et
al., 1993
Kapperud et al.,
1996
Kapperud et al.,
1996
Kapperud et al.,
1996
Klun et al., 2006
Rodrìguez-Ponce et
al., 1995
Smith, 1991
January 2008
Country
USA
USA
USA
USA (Illinois)
USA
USA
Worldwide
Several
surveys
Several
surveys
Several
surveys
Number
tested
Animal tested
5,936
2,449
382
30
93
1264
4252
2617
391
188
18
128
95
61
1243
1897
3479
73,717
Sheep
Goats
Black tailed deer
White tailed deer
Bison
Pigs
Pigs – finishing
Pigs – sows
Cats
Raccoons
Skunks
Opossums
Rats
White footed mice
House mice
Domestic pigs
Pigs
Pigs
5,862
Sheep
Percentage
seropositive
to 69)
37
23
20
3
3.1
0.9*
2.3
15.1
68.3
67.0
38.9
29
6.3
4.9
2.1
47.4
19.5
22 (range 0 to
97)
21
Reference
2,795
Goats
25
Smith, 1991
2,747
Horses
14.7
Smith, 1991
Smith, 1991
Smith, 1991
Smith, 1991
Smith, 1991
Smith, 1991
Dubey et al., 1997
Dubey et al., 1995
Gamble et al., 1999
Patton et al., 1997
Smith, 1991
Smith, 1991
NS = Not Stated
* The low seroprevalence in these results is attributed to the lack of cats on the remote island where these feral
pigs were tested, the presence of only one domestic cat was known on the island.
5.4.2
Prevalence in animal tissue
Pork has been regarded as the major vehicle for transmission of T. gondii infections in
humans. Data has shown however that with the shift from small outdoor farms to modern
intensive indoor rearing systems in Europe and North America, the prevalence in young
market-weight pigs has been declining and pork consumption is unlikely to still be a major
risk factor for toxoplasmosis (Dubey 1996c; Tenter et al., 2000). A small isolated farm in
Massachusetts where modern methods were not used appears to support this view as 93%
(51/55) of the 6 month old pigs harboured viable T. gondii cysts (Dubey et al., 2002a).
Prevalences in fattening pigs in several EU countries was reported to be <1% (Tenter et al.,
2000). In Zimbabwe, seroprevalence was lowest in commercial farms practicing good
hygiene (19.75%, n=238) and highest in backyard scavenging pigs (35.71%, n=70). The
authors concluded that modern intensive husbandry systems were important in reducing T.
gondii infection in domestic pigs (Hove et al., 2005).
Data reported in reviews of analyses for T. gondii in animal muscle tissue are summarised in
Table 8. Dubey (2000) has suggested that a higher risk of T. gondii in women who ate raw
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
27
January 2008
sausages, salami and other cured meats could be explained by the higher prevalence of the
organism in older animals that are more commonly used for such products.
Table 8:
Country
Reported prevalence of T gondii cysts in overseas animal tissue
Brazil
No.
tested
149
Canada
2,800
England
67
UK
71
USA
50
60
86
55
2094
2094
2094
NS
NS
4,302
7,313
Meat tested
Fresh pork
sausage
Pig heart and
diaphragm
Ready-to-eat
cured meats
Retail meat;
consisting of
57 pork
9 lamb
4 beef
1 beef/pork
Pig diaphragm
Beef cattle
diaphragm
Sheep diaphragm
%
positive
8.7
0
1.5
38
33
67
25
100
24
1.7
9.3
Pigs -6 month old
- hearts and
tongues (isolated
small farms)
Beef
Chicken
Pork
92.7
Cattle
Pig (most samples
were not of edible
tissue)
5
10
0
0
0.33
Assay
Method
Mouse
bioassay
Mouse
bioassay
PCR*/Tissue
culture
PCR*
Reference
Mouse
bioassay
Mouse
bioassay
Mouse
bioassay
Cat bioassay
Jacobs et al., 1960
Cat bioassay
followed by
further cat
and mice
bioassay
NS
NS
Dias et al., 2005
Gajadhar et al., 1998
Warnekulasuriya et
al., 1998
Aspinall et al., 2002
Jacobs et al., 1960
Jacobs et al., 1960
Dubey et al., 2002a
Dubey et al., 2005
Smith, 1991
Smith, 1991
NS = Not Stated
*PCR methodology detects presence of T. gondii DNA, not the presence of viable cysts.
In the Dubey et al. (2002a) study, the samples were obtained from 55 pigs destined for
human consumption. Five hundred grams of heart and tongue material were fed to 55 T.
gondii-free cats. Fifty-one cats (92.7%) shed 25 – 810 million T. gondii oocysts in their
faeces. In a surprising finding, further analysis found that two of the infected cats had eaten
apparently seronegative pig tissue (tests carried out were the Sabin-Feldman dye test,
modified agglutination test and the Western blot test). This suggests that these tests are not
entirely effective. The authors concluded that all meat should be cooked to industry
guidelines before human consumption.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
28
January 2008
In conclusion, the data presented in Tables 7 and 8 tend to suggest that prevalences obtained
when testing for cysts are lower than those obtained by serological tests. However, testing by
PCR (Aspinall et al., 2002) has shown, in one study at least, prevalences similar to those
found by serology. This suggests that the method used can influence the results and it is not
possible to say which is the “true” measure.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
29
January 2008
6
RISK CHARACTERISATION
Analysis of sera for infection determines the presence of IgG or IgM classes of antibodies
specific for a Toxoplasma antigen. The presence of IgG antibodies (which persist in the body
for long periods) indicates previous infection. IgM antibodies are a more recently available
test, and this class of antibody rises early in infection. For infections with most other
pathogens, IgM disappears in the weeks following primary infection. However, screening for
toxoplasmosis is unusually difficult because of the persistence of the IgM antibody response.
After primary T. gondii infection, IgM antibody frequently remains positive for many months
or even years and may falsely indicate a recent infection (Morris and Croxson, 2004).
Seroconversion in pregnant women refers to cases where IgG and IgM are absent prior to
conception, but appear in blood samples following delivery, thus demonstrating infection
during pregnancy.
6.1
Adverse Health Effects in New Zealand
6.1.1
Incidence and outbreaks
An early investigation of toxoplasmosis in New Zealand was undertaken by Manning and
Reid (1956). Sera from blood donors and student nurses (age range 16 – > 56 years) were
collected and tested for antibodies using the Sabin-Feldman dye test – see Table 9. This test
uses live virulent tachyzoites of T. gondii as the antigen to a series of dilutions of the test
serum thus measuring the total amount of antibody in the test serum capable. The results
show an increase in the percentage positive with age. Titre levels were also determined and
were found to be higher in the younger age groups reflecting the more recent infection status.
Sera from 9-year-old children from one school were also tested. Results are shown in Table
10. The number of positive results was considered unexpectedly high by the authors.
Table 9:
Dye test results (student nurses and blood donors)
Age group
Sex
No. tested (total)
No. positive (%)
16-25
M
F
M
F
M
F
M
F
M
F
M
F
25
45
35
30
31
23
24
25
9
11
124
134
7 (28)
12 (27)
16 (46)
14 (47)
15 (48)
15 (65)
14 (58)
13 (52)
6 (67)
7 (64)
58 (47)
61 (46)
26-35
36-45
46-55
Over 56
Total
Overall percentage
positive
27%
47%
56%
55%
65%
46%
Adapted from Manning and Reid, (1956)
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
30
January 2008
Table 10:
Sex
Male
Female
Total
Dye test results (nine year old school children)
No tested
No positive (%)
22
33
55
9 (41)
9 (27)
18 (33)
No. positive at reciprocal titre
16 32 64 128 256 512
- 1 3 3
2
- - 2
2 1
4
1 2
5 4
6
Adapted from Manning and Reid, 1956.
In respect to congenital toxoplasmosis, the incidence is unknown and New Zealand currently
has no routine antenatal serological screening for T. gondii infection.
A study of the incidence of toxoplasmosis in pregnancy in New Zealand reported that New
Zealand Health Information Service discharge data for ten years (probably 1989 to 1999)
indicated only 27 cases of toxoplasmosis in women of child bearing age (Moor et al., 2000).
Toxoplasmosis was a notifiable disease in New Zealand from 1987 to 1996. Only one case
of congenital toxoplasmosis was notified during this period (in 1990). This low notification
rate has been ascribed to under-reporting, as exemplified by National Health Institute data
that indicate, in 1988, nine diagnoses of clinical and serological toxoplasmosis were made in
babies (Moor et al., 2000).
The International Statistical Classification of Diseases and Related Health Problems 10th
Revision (ICD-10) is a coding of diseases signs, symptoms etc developed by the World
Health Organisation (WHO). The following ICD-10 codes relate to toxoplasmosis:
B 58
Toxoplasmosis (excludes congenital toxoplasmosis)
B58.0 Toxoplasma oculopathy
B58.1 Toxoplasma hepatitis
B58.2 Toxoplasma meningoencepthalitis
B58.3 Pulmonary toxoplasmosis
B58.8 Toxoplasmosis with other organ involvement (myocarditis, myositis)
B58.9 Toxoplasmosis unspecified
P 37 Other congenital infectious and parasitic diseases
P37.1 Congenital toxoplasmosis due to hydrocephalus
Table 11 shows the number of cases discharged from public hospitals from 2000 to 2006 with
a primary diagnosis of toxoplasmosis and a breakdown of the different clinical manifestations
in terms of ICD 10 code (Chris Lewis, New Zealand Health Information Service, personal
communication, 2007). Readmissions of the same patient have been excluded.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
31
January 2008
Table 11:
Public hospital discharge records for other acquired toxoplasmosis
manifestations by year, gender and age range
B58.0 Toxoplasma oculopathy
Year
2000
2001
2002
2003
2004
2005
2006
Total: 26
B58.2
Toxoplasma 2003
meningoencepthalitis
2004
2006
Total: 4
B58.3
Pulmonary 2001
toxoplasmosis
2004
2005
Total: 4
B58.8 Toxoplasmosis with 2000
other
organ
involvement
(myocarditis, myositis)
2003
2004
2005
Total: 13
B58.9
Toxoplasmosis 2000
unspecified
2002
2003
2004
2005
2006
Total: 37
Total for B58: 84
Male
4
1
0
3
2
4
1
15
1
Female
0
0
4
0
1
4
2
11
0
Age range
7-57
44
22-71
24-62
3-51
18-64
11-43
38
1
0
2
0
0
2
2
1
56
36-55
0
1
1
2
1
1
3
1
35
23-52
2
2
3
9
4
0
0
3
4
2
43-55
36-67
22- 44
3
3
3
5
6
24
51
2
2
1
3
3
13
33
42
33-86
36 – 48
27 – 57
11 – 40
21 – 41
21 – 54
1 – 50
H32.0 (chorioretinitis) was a secondary diagnosis in 11 of the cases with a primary diagnosis
of toxoplasma oculopathy r recorded from 2000 to 2006. H22.0 (iridocyclitis) was secondary
in 5 of the cases.
Toxoplasmotic meningoencephalitis was listed as a contributory factor in two HIVassociated deaths, one in each of the years 2001 and 2003.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
32
January 2008
In terms of congenital diagnoses records, as a primary diagnosis of P37.1, there were 3
fatalities recorded, all females in the years 2000, 2001 and 2003. Two were neonates while
one was 16 years old. For hospital discharges, there were 3 cases recorded in 2000, and 1
each in years 2001, 2002, 2003 and 2006, all neonates (Chris Lewis, NZHIS, personal
communication, 2007).
Metcalfe et al. (1981) reported on IgG levels to Toxoplasma in populations in Auckland,
Hamilton, Taranaki, Wellington and Napier/Hastings in the period of 1976 to 1978. Overall
45% of females and 48% of males had antibody titres that suggested prior infection
(reciprocal antibody titres of 64 or greater).
A survey of 566 pregnant women in Hamilton (Cursons et al., 1982) reported the prevalence
of antibodies to T. gondii as shown in Table 12.
Table 12:
Reported prevalence of Toxoplasma gondii antibodies in pregnant women
in Hamilton
Age Group and
number (n=566)
15-20, n=123
21-25, n=203
26-30, n=168
31-35, n=54
>35, n=18
Percentage of
sample population
Positive for
antibody
(%)
58.5
57.1
60.0
68.5
56.0
21.7
35.9
29.7
9.5
3.2
Seroconversion rate
estimated
(% per annum)
0.6
1.7
-
Based on these and earlier data, a seroconversion rate of 0.62% per annum has been
calculated, which was used as the basis for a further calculation to predict that 164 maternal
infections could be expected annually resulting in 66 foetuses becoming infected (Moor et
al., 2000). Actual diagnoses of Toxoplasma infection in pregnant women are much lower;
the same study reported that although 12% of live births occur in the Wellington region, only
10 cases of toxoplasmosis in pregnancy were diagnosed in Wellington from 1989 to 1997. It
was suggested that this discrepancy was “due in part to the relatively asymptomatic nature of
Toxoplasma infection and in part to a lack of awareness amongst many of the caregivers”.
These analyses do not include any information to indicate whether the infection was acquired
from food (undercooked meat) or other sources, particularly cats or soil in which cats have
defecated.
A study involving pregnant women submitting their first routine set of antenatal blood tests
in Auckland in 2000 tested 500 serum samples across five age groups, 100 samples per age
group (Morris and Croxson, 2004). Results are shown in Table 13. Testing was conducted
for both IgG and IgM antibodies.
Table 13:
Seropositivity in blood samples from pregnant women Auckland, n=500
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
33
January 2008
Age group (years)
<20
21 – 25
26 – 30
31 – 35
>36
All ages
IgG positive (%)
36
24
29
34
40
33
IgM positive (%)
4
5
0
2
1
2.4
The authors used these data, along with the numbers of births to women in these age ranges
in the Auckland region, to estimate that up to 2.2% of women could have initial antenatal
serology consistent with recent infection. Infections during the first trimester have a 10%
chance of being transmitted to the foetus, suggesting that 2 cases of first trimester congenital
toxoplasmosis could be occurring per 1000 pregnancies in Auckland. However, this level of
clinical disease is not currently being detected. Due to the potentially unnecessary anxiety
that antenatal screening might cause, and the uncertain benefit of medical interventions, the
authors concluded that antenatal screening for T. gondii is not currently justified in New
Zealand and that risk communication is the preferred option.
6.1.2
Clinical consequences of toxoplasmosis infection and people with AIDS
Toxoplasmosis is a potentially important infection for people with AIDS. Opportunistic
infection was a concurrent main clinical indicator for 570 of the 891 people notified with
AIDS from 1983 to 2005 in New Zealand (either living or dead). A specific infection is not
always reported, but toxoplasmosis or T gondii encephalopathy was reported for 13 of these
570 cases (Sue McAllister, Otago University, pers. comm., October 2006).
6.1.3
Case control studies and risk factors
No case control studies or risk factor studies have been conducted in New Zealand.
6.2
Adverse Health Effects Overseas
6.2.1
Incidence
It has been suggested that nearly one third of humanity has been exposed to T. gondii (Hill et
al., 2005; Dubey and Beattie, 1988). In the UK and USA, 16 – 40% of people are considered
to be infected, while in Central and South Amercia and continental Europe infection spans 50
– 80% of the population (Dubey and Beattie, 1988; Smith, 1997). Joynson (1992) estimated
the overall rate of toxoplasmosis in the UK as between 23 and 33% with regional differences.
With age, seropositivity increases by 0.5-1% until 50% of people are infected by the time
they reach 60 years old.
Sukthana (2006) collated the seropositivity rates in Europe, the Americas and Southeast Asia.
Additional surveys found have been added to this table and are presented in Table 14. It is
difficult to comment on these rates due to the differences in ages, tests and range of results.
However, in general, Western Europe rates are below 50% (except for France). Scandinavian
countries and the USA have low seropositivity rates at generally below 30%, while South
American countries and African countries report the highest rates (generally above 50%).
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
34
January 2008
In the India survey (Joshi et al., 1998), the dietary habits (vegetarians and non-vegetations)
were also examined with respect to seropositivity rates. No statistical differences were
found.
The seropositivity rates in the African studies are all over 43% except for Niger (18%). It
appears that the prevalence of toxoplasmosis was higher in humid coastal regions as opposed
to the drier inland desert areas.
Worldwide, the number of cases of congenital toxoplasmosis have been estimated at between
140,900 and 1,127,200, based on an estimated rate of 0.1 to 0.8% of 140.9 million live births
in 1992 (Roberts et al., 1994).
Table 14:
Seropositivity rates overseas in humans
Countries
Western Europe
Austria
Belgium
France
Germany
Italy
Netherlands
Spain
Switzerland
UK
Scandinavia
Denmark
Finland
Norway
Sweden
Central
&
Eastern Europe
Croatia
Poland
Slovenia
The Americas
USA
Central America
Costa Rica
Year
Seropositivity (%) References
1998
1990
2004
1996
2004
1990-91
-
43
50
up to 75
26-54
18-60
40.5
28.6
46
23-33
1999
1995
1992-94
2001
27.8
20.3
10.9 (preg. women)
56.6 (women)
21.8 (military rec.)
14.0-29.4
1996-99
36.4
46.4-58.5
34 (preg. women)
Tonkic et al., 2002
Sroka, 2001
Logar et al., 2002
2004
1999-2000
1988-1994
1988-1994
1988-1994
9.9 (military rec.)
16-40
15.8 (aged 12-49)
22.5 (age > 12)
15 (women 15-44)
25.4 (age > 20)
(males -26.2)
(females - 24.7)
Smith et al., 1996
Dubey, 2004
Jones et al., 2003a
Jones et al., 2001
1996
76
Arias et al., 1996
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
35
Moese and Vander-Moese, 1998
Luyasu et al., 1997
Tenter et al., 2000
Gross, 2004
Tenter et al., 2000
Kortbeek et al., 2004
Munoz Batet et al., 2004
Jacquier et al., 1995
Joynson, 1992
Lebech et al., 1999
Lappalainen et al., 1995
Jenum et al., 1998
Smith, 1991
Smith, 1991
Evengård et al., 2001
Kruszon-Moran
2005
&
McQuillan,
January 2008
Countries
Cuba
Mexico
Panama
South America
Venezuela
Argentina
Brazil
West Indies
Asia
Indonesia
Malaysia
India
China
Japan
Africa
Nigeria (Ibadan)
Nigeria (S. Delta)
Somalia
Niger
Egypt
Year
1987
1988
Seropositivity (%)
29.7
35
90 (at age 60)
References
Machin Sanchez et al., 1993
Tenter et al., 2000
Sousa et al., 1988
1991
-
63
72
59
57
45 (1-19 yrs)
Diaz-Suarez et al., 2003
Tenter et al., 2000
Tenter et al., 2000
Prabhakar et al., 1991
Rawlins and Prabhakar, 1989
-
58a
44.8
1.5 – 21
17.2
0.7
2.9 (Age 20-29)
40 (Age 70-90)
29 (males)
16 (women)
Konishi Houki et al., 2000
Nissapatorn & Abdullah, 2004
Mohan et al., 2002
Joshi et al., 1998
Smith, 1991
Smith, 1991
-
78 (preg. women)
83
44
18
43
Jones et al., 2001
Jones et al., 2001
Jones et al., 2001
Julvez et al., 1996
el-Nawawy et al., 1996
a male:female ratio = 63:52
6.2.1.1 USA
It has been estimated that 0.6% of the US population experiences an acute toxoplasmosis
infection each year, representing approximately 1,500,000 infections per year (Mead et al.,
1999). The USDA estimate that 50% of T. gondii infections are caused by raw or
undercooked meat consumption (Buzby and Roberts, 1996), and a community-based
Maryland study comparing meat eaters with non-meat eaters supports this assumption
(Roghmann et al., 1999). This means that an estimated 750 deaths per annum are due to
toxoplasmosis and, if one half or 375 deaths are due to raw or undercooked meat, then
toxoplasmosis ranks as the third leading cause of foodborne deaths in the USA (Mead et al.,
1999).
Jones et al. (2003a) and Lopez et al. (2000) have estimated a range of between 400 and 4,000
cases of congenital toxoplasmosis each year in the USA.
Toxoplasmic encephalitis occurs in approximately 7% of USA AIDS patients, although this
proportion declined from 1992 to 1997 (Schwartzman, 2001). A worldwide proportion of
10% has been estimated for the number of AIDS patients that die due to toxoplasmosis, while
the equivalent figure in Europe has been estimated as 30% (Luft and Remington, 1992 cited
in Hill and Dubey, 2003).
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
36
January 2008
6.2.1.2 Europe
The Eurotoxo project, launched in 2002, is a European consensus initiative that has worked
to provide a consensus on the current state-of-science knowledge on toxoplasmosis. The aim
is to construct a research agenda from current knowledge so that policy decisions can be
made that best prevent congenital toxoplasmosis and its consequences (See website:
European
Toxo
Prevention
Project
http://eurotoxo.isped.ubordeaux2.fr/WWW_PUBLIC/US-EUROTOXO-PublicAccess-Frame.htm).
In 2004, the European Food Safety Authority collected data from 25 member states and
Norway covering 11 zoonotic agents, including Toxoplasma (EFSA, 2005). Eighteen States
reported a total of 1,736 human cases of toxoplasmosis in 2004, 45 of which were registered
as congenital infections. Data for the years 2000 – 2003 were of a similar order. The overall
EU incidence was 0.6 cases per 100,000 population. As some countries only report certain
clinical aspects of the disease or do not report the illness at all, this rate is considered an
under-estimation. For further information on the characteristics of the European surveillance
systems, refer to the Eurotoxo survey on European surveillance systems (Bénard and Salmi,
2005).
The 2005 Zoonoses Report for the United Kingdom (DEFRA, 2006) reported that between
1998 and 2005 there was an average of 117 toxoplasmosis cases reported per annum directly
from National Health Service laboratories (total UK population in 2006 was 60.5 million).
There were also an additional 300-500 cases identified each year through the Toxoplasma
Reference Unit which captures the milder cases affecting the general population and also the
more severe, life-threatening symptoms affecting HIV/AIDS patients, organ transplant
recipients and unborn children.
The 2004-2005 British Paediatric Surveillance Unit Annual Report (BPSU, 2005; Gilbert et
al., 2006) included symptomatic toxoplasmosis in childhood to inform the debate on neonatal
screening. The research in the UK (Gilbert et al., 2006) studied 38 cases of toxoplasmosis
infected children (<16 years) between the years 2002 and 2004. Key points made were that
confirmed symptomatic cases were reported more often by opthalmologists (19 cases) than
by paediatricians (4) and the majority (22/38: 58%) were due to congenital infection, leaving
16/38 (42%) as post-natally acquired toxoplasmosis – all 16 had retinochoroiditis symptoms
and no other complications. All 16 children post-natally infected, presented after 4 years of
age, 14 of the 16 (88%) presenting at 10 or more years of age. In total, 31 of the 38 cases had
ocular toxoplasmosis, with almost half of these cases infected post-natally.
6.2.1.3 Australia
Toxoplasmosis is not a notifiable disease in Australia and there are few data on the incidence
of the disease. However, extrapolation of data from overseas (principally the USA – Mead et
al., 1999) has been used to estimate the extent of foodborne toxoplasmosis in Australia
(Australian Government, 2005).
Total cases
(95% Credible Interval (CrI))
17,100 (9,000 – 26,000)
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
% Foodborne
(95% CrI)
35 (0-71)
37
Foodborne illness
(95% CrI)
5,900 (0-13,900)
January 2008
This represents the majority of the estimated 6,000 cases of “other” (i.e. non-gastrointestinal)
foodborne illness in Australia.
Most other information concerning toxoplasmosis in Australia relates to the congenital form
of the disease. The annual number of cases of congenital toxoplasmosis in Australia has been
estimated as 534 (0.2% of 0.3 million live births) (Roberts et al., 1994). An early paper
(Sfameni et al., 1986) examined the case for antenatal screening for Toxoplasma amongst
other infections such as rubella and cytomegalovirus (CMV). The sera of 3,463 pregnant
women attending antenatal clinics in Melbourne were tested during a 12 month period from
March 1983. Prevalence of Toxoplasma antibody rose from 40.2% in women aged 16-20 to
54.8% in those aged 36-40. Over the 20 year span, the increase was 7.3/1000 women years
(5.5/1000 during a 9 month period) – a similar rate to the observed seroconversion rate.
A survey for congenital toxoplasmosis in Western Australia (Walpole et al., 1991) involved
approximately a quarter of infants born in the State. Sera from 10,207 pregnant women and
cord blood specimens from 18,908 infants were tested (7523 of these were linkable to
maternal sera). Fourteen infected mothers were identified (specific IgM antibodies present),
11 from maternal sera and 3 from the cord blood (0.23 per 1000 births to non-immune
mothers). Maternal immunity was indicated in 35% (3544/10207) at the first ante-natal visit.
Subsequent tests on the eleven cases indicated no serological or clinical evidence of
congenital toxoplasmosis in the offspring of these mothers. The rate of maternal infection in
susceptible pregnancies was calculated to be 1.6 per 1,000. The maternal-foetal transmission
rate was estimated at < 24%.
There were no clinical signs of congenital infection in the three infants associated with the
positive cord blood but long-term checks would be required. Thirteen of the 14 infected
mothers were interviewed, only three identified a known risk factor. The authors concluded
that an ante natal toxoplasmosis screening programme was not justifiable in Western
Australia.
6.2.1.4 Worldwide data for seroconversion during pregnancy
Worldwide, data for seroconversion during pregnancy from a number of studies are
summarised in Table 15. Kemmeren et al. (2006) calculated from a number of studies in the
Netherlands, a prenatal infection rate from mother to foetus of 23 per 10,000 births.
Table 15:
Seroconversion rates during pregnancy for T. gondii infection
Country
Number tested
Australia
(Western)
10207 women
18,908 cord blood
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
Seroconversion
(%)
1.6 per 1000
38
Reference
Walpole et al., 1991
January 2008
Denmark
England
England
NS
1621
13328
Finland
France
France
NS
7605
951
Norway
Sweden
USA
World
NS
NS
3094
NS
NS
95929
0.21
0.023
3-16 infected foetuses per
100,000 pregnancies
0.24
0.1
Native French 2.3
Immigrant 1.6
(probability of infection)
0.17
0.13
0.38-0.75 (estimate)
0.1-0.8 (estimate)
0.5
Evengård et al., 1999
Zadik and Siddons, 1995
Allain et al., 1998
Evengård et al., 1999
Smith, 1991
Smith, 1991
Evengård et al., 1999
Evengård et al., 1999
Roberts and Frenkel, 1990
Murrell, 1995
Smith, 1991
NS = Not Stated
6.2.2
Contribution to outbreaks and incidents
Sukthana (2006) has collated information on the percentage of Toxoplasma infections
associated with meat in Europe (Table 16). This information suggests that pork is less
important than other red meat types as a transmission vehicle for tissue cysts.
Table 16:
Percentage of human toxoplasmosis associated with meat types consumed
Country
1
Belgium
Denmark1
Italy1
Norway1,2
Switzerland1
Percentage
Beef
6
27
12.5
19
8
Pork
2
2
3
3
13
Lamb
10
8
0.5
21
10
Salami
10
4
12.5
3
5
1 Cook et al., 2000, 2 Kapperud et al., 1996
Source: Sukthana (2006).
Reported outbreaks of foodborne toxoplasmosis associated with rare meat are summarised in
Table 17.
Table 17:
Country
Australia
Australia
Summary of information on outbreaks of infection with T. gondii
associated with raw or rare red meat
Number of
cases
5
12
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
Implicated Meat
Reference
Raw lamb
Undercooked kangaroo
Smith, 1993
Robson et al., 1995
39
January 2008
Brazil
Canada
England
England
Korea
Korea
USA
USA
USA
USA
USA
USA
95
4
3
1
3
5
2
1
3
6
4
5
Rare meat (hamburger?)
Raw seal and/or caribou
Raw lamb
Raw or rare steak
Raw pig liver and spleen*
Raw pig liver*
Rare meat
Rare meat
Rare/raw venison
Rare lamb
Raw beef
Rare meat (hamburger)
Smith, 1993
McDonald et al., 1990
Smith, 1993
Smith, 1993
Choi et al., 1997
Choi et al., 1997
Smith, 1993
Smith, 1993
Sacks et al., 1983
Smith, 1993
Smith, 1993
Smith, 1993
* Although offal, these entries are included in the table for information.
A search of the Pubmed database (21.11.06) did not locate reports of any further outbreaks
associated with meat.
An outbreak of toxoplasmosis associated with a municipal drinking water facility has been
reported in Victoria, Canada (Bowie et al., 1997). Domestic cats and cougars living in the
area of the surface water reservoir were shown to be shedding oocysts (Aramini et al., 1999).
The water supply was unfiltered, and although disinfection using chloramination was used,
this method is unproven against T. gondii.
An outbreak between November 2001 and January 2002 in Brazil was linked to contaminated
water and commercial ice cream prepared with the water (de Moura et al., 2006). An
unfiltered municipal treated water supply was epidemiologically linked to and confirmed by
PCR as the source of the outbreak. A litter of kittens delivered and living on top of the
reservoir tank fitted the timeframe of contamination. Cracks in the roof of the reservoir
allowed rainwater penetration and possibly infected cat faeces through into the reservoir. In
addition, chlorination levels were inadequate to destroy the oocysts. Confirmation of T.
gondii in the kittens could not be made as the kittens could not be caught.
6.2.3
Overseas studies
A key cohort study overseas is part of the Eurotoxo project. The study includes 1200
toxoplasma-infected women, spread over 15 centres in 7 countries in Europe and Brazil. The
women in the study were recruited between 1997 and 1999, enabling a long term study of the
children born subsequently. In particular, risks of transmission, signs of damage and effect
of prenatal treatments have been looked at. The project has already resulted in a number of
publications, these are listed on a website link to the European Multicentre Study on
Congenital Toxoplasmosis;
http://www.ucl.ac.uk/paediatric-epidemiology/EMSCOT/emscot.html.
A systemic review of risk factors for T. gondii infection in pregnant women is also part of the
Eurotoxo project. This review identified four case-control studies, the findings are
summarised below, as well as a recently published English study. The Eurotoxo authors
concluded that case-control studies are not the best evidence on which to investigate risk
factors, especially using personal retrospection that introduces recall bias. From these
studies, risk factors vary according to local food customs, food hygiene and lifestyles. The
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
40
January 2008
authors thought that a “transversal” designed study was of greater benefit (i.e. prospective,
information on both risk and disease infection collected simultaneously). Only one such
study was found by the review: conducted in Serbia-Montenegro conducted between 1988
and 1991 (Bobic et al., 1998). The study of 1157 reproductive age females (15years-49
years) in Belgrade found that undercooked meat consumption and exposure to soil were
significant, while ownership of cats had no influence.
A case control study in France investigated risk factors for Toxoplasma infection in
pregnancy (Baril et al., 1999). A total of 80 pregnant women who seroconverted to
Toxoplasma were matched with 80 pregnant women who had repeatedly negative tests. The
risk factors determined from a multi-variate analysis were:
•
•
•
Consumption of undercooked beef OR=5.5 (95% CI 1.1-27);
Having a pet cat OR=4.5 (95% CI 1.0 – 19.9);
Frequent consumption of raw vegetables outside the home OR 3.1 (95% CI 1.2 – 7.7).
Undercooked meat was defined in this study as rare if the centre of the meat was still raw and
medium if the centre was still pink.
Insufficient numbers of study participants reported consumption of undercooked pork to
determine an odds ratio. Poor handwashing (OR=9.9, 95% CI: 0.8 – 125), and consumption
of undercooked lamb (OR=3.1, 95% CI 0.85 – 14) had elevated but not statistically
significant odds ratios in the multi-variate model. Receipt of documentary advice on
prevention was associated with a lower risk of infection.
A study in Naples (Buffolano et al., 1996) was conducted with pregnant women who were
interviewed with regard to risk factors and tested for their levels of serum anti-Toxoplasma
IgG and IgM antibodies. The levels of these were used to determine the time of infection
(IgM positive and IgG positive = recently infected, IgG negative = susceptible and IgM
negative, IgG positive = previously infected). Complete results were available for 3518
women, of whom 42 (1.2%) were recently infected, 1380 (39%) were previously infected and
2096 (60%) were susceptible.
Compared to the susceptible group, recent infection (i.e. IgM positivity) was associated with:
•
•
•
Eating cured pork (more than once a week or once a month) OR 2.9 (95% CI 1.6-5.5)
Eating raw meat (more than once a week or once a month) OR 2.6 (95% CI 1.4-4.7)
Gardening (once a week or once a month) OR 2.0 (95% CI 1.1-3.7)
Parity, rural/urban residence, living on a farm, or owning a cat were not significant. This was
the first report identifying cured pork as a significant risk factor for recent Toxoplasma
infection. The authors recommended further studies to confirm this association and to
determine viability of tissue cysts in cured pork products. There was also a dose dependent
response between frequency of consumption of cured pork (weekly or monthly) and raw meat
and the odds ratio.
A prospective case control study using similar criteria to that of the Naples study for defining
cases was carried out in Norway from 1992 to 1994 (Kapperud et al., 1996). From 37,000
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
41
January 2008
pregnant women, a total of 63 women with recent primary infection and 128 seronegative
controls were matched. The independently associated risk factors were:
•
•
•
•
•
•
Eating raw or undercooked minced meat products
OR 4.1 (95% CI 1.5-11.2)
Eating unwashed raw vegetables or fruits
OR 2.4 (95% CI 1.1-5.6)
Eating raw or undercooked mutton
OR 11.4 (95% CI 2.1-63.1)
Eating raw or undercooked pork
OR 3.4 (95% CI 1.1-10.4)
Cleaning cat litter box
OR 5.5 (95% CI 1.3-22.7)
Washing the kitchen knives infrequently after preparation of raw meat, prior to handling
another food item
OR 7.3 (95% CI 1.1-50.2)
More recently a multi-centre study in Europe again used seroconversion to define cases (n =
252), which were compared with controls (n = 852) (Cook et al., 2000). The following
factors were the most strongly predictive of acute infection in pregnant women;
p value
• Eating raw/undercooked beef
OR 1.73 (95% CI 1.1-7.2)
0.01
• Eating raw/undercooked lamb
OR 3.13 (95% CI 1.4-7.2)
0.007
• Eating “other”* meat
OR 4.12 (95% CI 1.6-10.9) 0.004
• Contact with soil
OR 1.81 (95% CI 1.2-2.7)
0.005
• Travel outside of Europe/USA or Canada
OR 2.33 (95% CI 1.3-4.1)
0.003
* specifically venison, horse, rabbit, whale and game birds
Weaker associations (p>0.05) were observed for tasting meat during meal preparation, eating
salami, drinking unpasteurised milk and working with animals. Contact with cats, kittens, cat
faeces or cats who hunt for food were not identified as statistically significant risk factors,
possibly because the excretion of oocysts after infection is limited to only a few weeks.
Between 30 and 63% of the infections could be attributed to meat consumption (including
cured meats), and 6 to 17% to contact with soil.
A case control study in Jordan compared seropositive (n = 132) and seronegative (n = 148)
pregnant women (Jumaian, 2005). Consumption of undercooked meat (p<0.0001) and
contact with soil (p<0.022) were significant risk factors, whereas ownership of a cat was not.
6.2.4
Risk assessments overseas
A probabilistic model that describes incidence of the disease has been developed but only a
conference abstract has been located (Cassin et al., 1996). In discussion of this model
(Lammerding and Paoli, 1997), three key factors are reported as being simulated: cat
ownership, consumption of implicated products, and the age distribution of pregnancy. Note
that the majority of case-control studies already discussed, do not cite cat ownership as a risk
factor.
Two models to estimate the incidence of toxoplasmosis in the UK have been published. A
model to estimate time and age-specific incidence was based on 3,785 blood samples
collected from patients aged 2 – 100 in South Yorkshire, England between 1969 and 1990
(Ades and Nokes, 1993). The results showed that incidence appeared to have fallen sixfold
between 1915 and 1970, remaining stable in the following 20 years up to 1990. The
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
42
January 2008
incidence was higher in children than in adults, and in women throughout the childbearing
period was estimated as 0.07 or less per 100 susceptible persons.
A recent study (Nash et al., 2005) established the relative importance of risk factors for an
antenatal population in England. Toxoplasma immune status was determined by
immunoassay, and a questionnaire investigated dietary and environmental factors of 1897
women. Seroprevalence was 172/1897 (9.1%) confirming that the prevalence of infection
has continued to decline since the 1960s (Ades and Nokes, 1993; Joynson, 1992; Walker et
al., 1992). A significantly higher seroprevalence was associated with;
•
•
•
•
Rural location of childhood home;
Childhood home in Europe (excl. UK);
Feeding a dog raw meat;
Increased age.
Living with a cat or kitten as a child resulted in a non-significant higher prevalence.
In contrast to mainland European studies, there were weak associations with diet. Table 18
displays the red meat consumption and raw meat handling factors investigated in the study:
Table 18:
Relative importance of risk factors for an English antenatal population
Question
Response
Eaten beef, pork or lamb Yes
in the past 10 years?
No
How was beef eaten?
Not eaten
Rare
Medium
Well done
How was pork eaten?
How was lamb eaten?
Not eaten
Rare
Medium
Well done
Not eaten
Rare
Medium
Well done
Often fed cat/kitten raw No
meat
Yes
Often fed dog raw meat
No
Yes
Smoking while handling No
raw meat
Yes
Cases
sero
+ve
166
4
9
14
36
111
Cases
sero
-ve
1641
79
131
96
332
1163
12
2
6
150
22
1
18
129
172
3
25
1522
233
6
134
1349
143
28
138
34
167
5
1540
177
1528
189
1683
25
RR
95% CI
1.91
0.72-5.01
P
value
0.245
0.346
2.12
1.58
1.39
0.88-5.1
0.74-3.36
0.69-2.8
9.56
3.44
1.41
1.46-62.76
1.19-9.98
0.77-2.59
1.77
1.42
1.01
0.20-15.33
0.74-2.75
0.63-1.63
0.043
0.624
1.10-2.35
1.61
0.856
1.84
1.30-2.61
1.85
0.82-4.16
0.650
0.188
RR = Relative risk, CI = Confidence interval
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
43
January 2008
There were weak associations with eating undercooked or medium-cooked pork that were not
significant after logistic regression. There was a significant association with feeding a dog
raw meat but no association between feeding the same to a cat or kitten. There was no
association with handling raw meat in the kitchen but there was a non-significant association
between smoking and handling of raw meat.
The consumption frequency of meats was also investigated and associations were apparent
with beef tongue (P=0.092), lamb chops (P=0.085), beefburgers (P=0.018) and cured pork
products (P<0.001) but after multi-variate logistic regression, the results were not significant.
A single multi-variate analysis was also carried out on the preference for 18 fresh and frozen
food purchases prior to their pregnancies. For 15/18 products where the preference was
frozen, the women had a lower relative risk for seropositivity than a preference for fresh
food. Frozen purchases with a higher relative risk were beef tongue, pork roast and lamb
roast. There was no attempt to determine whether a valid statistical difference occurred
between fresh versus frozen products because no valid statistical method could be found by
the authors.
6.3
Estimate of Risk for New Zealand
The reported seroprevalence of antibodies to Toxoplasma infection in New Zealanders varies
from 25 - 65% in male and female adults in the 1950s, 56 - 68% in pregnant women in a
study in the early 1980s, and 33% in pregnant women in Auckland in 2000. These
percentages are in keeping with reports for seropositivìty in Europe and the USA (Table 14).
In the Netherlands the seropositivity in 1996 was estimated to be 40.5% (Kemmeren et al.,
2006). Estimates of seroconversion in pregnant women for New Zealand are similar to those
for overseas (Table 15).
Data on the prevalence of infection of animals in New Zealand are scant, and no surveys of
meats have been found. Data on the prevalence of infection in overseas animals are quite
variable and this precludes the development of a proper exposure assessment. Further
research on the prevalence of infection of meat animals (particularly pigs) in New Zealand,
together with a survey to determine the presence of contamination (preferably with some
estimate of infectivity) in meat for retail sale, would be required for a proper risk assessment.
The multicentre case control study from Europe found that between 30 and 63% of T. gondii
infections could be attributed to meat consumption (including cured meats) (Cook et al.,
2000). Although pork is often cited as a high-risk meat, it is clear from the outbreak and case
control studies that other meats are also associated with transmission. Eating contaminated
food has been estimated to cause 50% of T. gondii infections in the USA (Mead et al., 1999).
Although data on the prevalence of antibodies in the blood of animals may over-estimate
infectivity, it seems likely that New Zealanders are exposed to infective cysts via
undercooked meat. However, there is no information currently available to link cases of
Toxoplasma infection with foodborne transmission, or to assess its importance relative to
other transmission routes.
6.4
Risk Categorisation
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
44
January 2008
The rationale for categorisation of food/hazard combinations is presented in Appendix 1.
The proportion of severe outcomes of Toxoplasma infection in immunocompetent people is
very low. However, the proportion of severe outcomes resulting from congenital
toxoplasmosis is significant at 5%, and so this infection has been assigned the highest
severity category. It is not possible to assign a category based on incidence, as there is
insufficient information on which to base such an assessment for New Zealand. However,
current reporting systems suggest that severe disease caused by T. gondii is very uncommon
in New Zealand.
6.5
Summary
Food/hazard
combination
Severity
Incidence
Toxoplasma
gondii in red
meat
and
meat products
1 (>5% serious
outcomes
for
congenital
toxoplasmosis)
Rare but robust
information
is
lacking
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
Trade importance
45
Other considerations
January 2008
7
RISK MANAGEMENT INFORMATION
When considering preventative measures for acquired toxoplasmosis, the culture and beliefs
of the population should be taken into account rather than giving orthodox health education
(Sukthana, 2006). This advice comes from the different transmission routes attributed
worldwide and whether direct ingestion of cysts via raw or undercooked meat is likely to be
important, or whether transmission stems from ingestion of oocysts from cat excreta in food
or soil. The subject of this Risk Profile is the direct ingestion of the cyst from red meat
animals.
7.1
Relevant Food Controls
Prevention or minimisation of infection with T. gondii, at least in pigs, appears to be possible
through the use of confinement systems for production. These include bird and cat-proofed
buildings, feed storage in enclosed silos, use of pelleted and heat-treated feed, not keeping
cats on finishing sites and regular rodent control programmes. Such measures have been
shown to almost eliminate seroprevalence in pigs in North Carolina (Davies et al., 1998).
Recommendations for the prevention of toxoplasmosis in the United States have been
published (Lopez et al., 2000). The recommendations were for the control of foodborne
pathogens in general, rather than being specific for Toxoplasma:
•
•
•
To cook meat to a safe temperature (internal temperature of 145°F (62.7°C) for beef,
lamb and veal roasts and steaks, 160°F (71.1°C) for pork, ground meat and wild game,
180°F (82.2°C) for poultry); (note that cooking temperature for poultry has since been
revised down to 165°F (73.8°C));
Peel or thoroughly wash fruits and vegetables before eating;
Clean cooking surfaces and utensils after they have contacted raw meat, poultry, seafood
or unwashed fruits or vegetables.
Smith (1991) has summarised the following advice from a number of authors to prevent T.
gondii infection in the home environment:
•
•
•
•
•
•
7.1.1
All meats should be cooked to at least 70°C, and meats not tasted during
preparation/cooking;
Hands, cutting boards, kitchen-tops, utensils should be thoroughly washed after
raw/undercooked meat contact. Do not touch mucous membranes (nose, eyes, mouth)
until hands are washed;
Thoroughly wash fruits and vegetables;
Protect food from cockroaches, flies or other insects;
Feed pets only dry, canned or thoroughly cooked foods;
Freeze meat to at least –12.5°C.
EFSA Review
The European Food Safety Authority provided an overview of their recommendations
concerning Toxoplasma gondii in a document published in 2007 (EFSA, 2007).
This stated:
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
46
January 2008
“Consideration of risk factors and public health priorities
•
•
•
The consumption of undercooked meat containing infective tissue cysts (bradyzoites)
and ingestion of infective oocysts (sporozoites) shed by cats in the environment are
the main risk factors.
Water containing infective oocysts may be an infection source or transmission vehicle
for humans.
Toxoplasma prevalence in livestock may be expected to rise due to an increase in
outdoor rearing of animals that, as a result, are more likely to come in contact with the
environmental infective stage (i.e. sporulated oocysts shed by cats).
Recommended actions to be taken to improve the protection of public and/or animal health
•
•
•
•
•
Intervention strategies should be enforced to reduce the access of Toxoplasma into the
food chain. In this connection hygiene conditions in animal husbandry and food
processing procedures have to be highlighted and observed.
Education campaigns with special focus on vulnerable groups such as pregnant
women and immuno-compromised persons are important so as to ensure that the risks
of acquiring Toxoplasma infection through contaminated food or from the
environment are addressed.
Networking between the Public Health and Animal Health sectors should be
improved in order to further understanding of the transmission and epidemiology of
Toxoplasma and toxoplasmosis. In outbreaks, tracing from fork to farm should be
improved in order to better identify the source of the infestation and put appropriate
control measures in place.
Case definitions of toxoplasmosis should be further developed and harmonised so as
to ensure a better comparison of data.
Sensitive, robust and reproducible Toxoplasma detection methods that are harmonised
and standardised, which are essential for efficient monitoring, require further
development.
Suggested improvements for monitoring and reporting
•
•
•
Although toxoplasmosis is known to be a very common infection this is not well
reflected in the available data. The collection of representative data on the disease
burden in human and the role of food, including water, in Member States is crucial for
any future decision regarding food safety intervention.
Serological methods should be standardised and harmonised for the monitoring of
food producing animals, and feasible methods for the routine detection of Toxoplasma
in meat, meat products and water should be developed and validated. This requires
the production and distribution of suitable reference materials.
Once such standardised methods are available, Toxoplasma monitoring should start
on pre-harvest sector in food-producing animals.”
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
47
January 2008
7.2
Economic Costs and Burden of Illness
The economic losses caused by congenital toxoplasmosis can be considerable. Estimates for
the USA range from US $0.4 – 8.8 billion, and for the UK from US $1.2 – 12 million
(Roberts et al., 1994; Roberts and Frenkel, 1990). The ranges are due to uncertainty as to the
actual number of infected babies. Medical costs are minor, while the majority of costs derive
from the value of statistical lives lost from neonatal death, and income losses by people with
long term physical and mental problems resulting from toxoplasmosis in infancy. The
differences in cost between the USA and UK are largely due to differences in the way income
losses are estimated.
As part of a priority setting exercise for foodborne pathogens in the Netherlands, an estimate
of the disease burden in disability adjusted life years (DALYs) has been published for both
congenital and post-natally acquired toxoplasmosis (Kemmeren et al., 2006). The DALY
estimate is the sum of years of life lost and years lived with disability, weighted for severity
of the illness. Disability weights were derived from Dutch studies. Although the long term
goal of the project was to estimate foodborne pathogens, for this estimate all illnesses were
counted, with no attempt to assign attribution according to source of infection.
For congenital toxoplasmosis the incidence of disease outcomes including stillbirth, a variety
of symptoms including chorioretinitis in the first year of life, and chorioretinitis later in life
were estimated. The incidence of congenital toxoplasmosis was derived from an estimate of
the number of women who were infected during pregnancy and the transmission rate, giving
an estimate of 8.2 (90% CI 4.9 – 12.2) per 10,000 live births (although an estimate from a
different study gave 23 per 10,000 live births). A variety of studies were then used to
estimate the incidence of the specific outcomes above.
For post-natally acquired toxoplasmosis, the incidence was back calculated from the
incidence of an outcome: ocular toxoplasmosis (chorioretinitis). Two hundred new cases of
ocular toxoplasmosis are reported annually in the Netherlands. Taking the estimate of 0.3%
that presented with symptoms in the Vancouver outbreak (Burnett et al., 1998), this equates
to an estimated 67,000 cases that contract acquired toxoplasmosis each year, an incidence
rate of 41 cases per year in the Netherlands.
Taking the estimate of 14% that have mild symptoms, 0.7% severe symptoms and 0.3% with
chorioretinitis, Kemmeren et al., then calculated the most likely number of cases and the
disease burden for the year 2004. The incidence for mild symptoms was estimated to affect
9300, severe symptoms (excl. chorioretinitis) 470 and chorioretinitis 200.
The cumulative disease burden for the Netherlands was then calculated for congenital and
acquired toxoplasmosis. The result was 2400 DALYs (1200 congenital DALYs per year
(range 520 – 2700) and 1200 acquired DALYS per year (range 40-2700)). Overall,
toxoplasmosis was the illness with the highest disease burden of those estimated, although it
also had the greatest uncertainty, resulting from poor information on incidence. At 1200
DALYs, the acquired toxoplasmosis disease burden was similar to that of campylobacteriosis
in the Netherlands.
No estimates of the economic cost or burden of illness to New Zealand from toxoplasmosis
have been located.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
48
January 2008
7.3
Other Transmission Routes
7.3.1
Toxoplasma in non-livestock animals in New Zealand
Cats: T. gondii uses cats as the definitive host, and a wide range of animals as intermediates,
including humans. The infection persists better as tissue cysts in intermediate hosts than in
the soil as oocysts (Frenkel, 1990). Most cats in New Zealand have antibodies to
Toxoplasma, indicating that they have been exposed to the parasite at some time during their
lives. The cats most at risk are immuno-suppressed adults or kittens that are seronegative
(Thompson, 1999).
Dogs: Reports of T. gondii infection in dogs are rare but the true prevalence may be hidden
by misdiagnosis. In New Zealand, T. gondii was isolated from a dog in 1956 (Hartley, 1956).
A retrospective New Zealand study of 15 cases of encephalomyelitis found two cases of T.
gondii infection. Using light microscopy Neospora cysts were indistinguishable from T.
gondii cysts, electron microscopy confirmed the differences (Patitucci et al., 1997).
Generally adult dogs are resistant while puppies are fully susceptible (Hill and Dubey, 2003).
Wallabies: Several outbreaks of toxoplasmosis have been reported in captive wallabies
(MAF 1974; 1980; 2000). In 1974, eight of 20 wallabies died over a two month period at
Christchurch zoo. In the most recent outbreak in 2000, three caged wallabies developed hind
limb paralysis over several months. A post-mortem on one of the animals revealed numerous
intact and ruptured cysts typical of Toxoplasmosis. No data were found on the prevalence in
feral populations of wallabies. Marsupials are apparently very susceptible to the disease,
while cattle and horses are among the most resistant hosts (Hill and Dubey, 2003).
7.3.2
Prevalence of T. gondii in cats overseas
Surveys of T. gondii in cats overseas have shown a prevalence range of 0% to 90%. A
summary of a selection of these surveys is below.
In Tehran, Iran, serum samples from 50 stray and 50 household cats revealed 90% of the
stray cats were seropositive compared to 36% of the household cats, giving an overall
infection rate of 63%. There was a high positive correlation between age and rate of
infection (Haddadzadeh et al., 2006).
In Adelaide, South Australia, faeces from 115 stray or unwanted cats were screened for T.
gondii. None contained detectable levels of viable oocysts. Alongside this study, 60 samples
of lamb and pork chops from 15 local butcher shops were also tested. No cysts were detected
other than one viable cyst in a pork chop (Rothe et al., 1985).
From Illinois, USA, faeces of 274 cats trapped on 47 pigs farms, together with samples of
feed and soil were bioassayed in mice for the presence of oocysts (Dubey et al., 1995). T.
gondii was isolated from five faecal samples (1.8%), 2 of the 491 feed samples (0.4%) and
one of the 70 soil samples (1.3%). The authors concluded that the possibility that T. gondii
could be transmitted to pigs via rodents, feed and soil was confirmed.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
49
January 2008
A range of wild mammals, cats, dogs and humans were tested in Chile, in the Juan Fernandez
Archipelgo (Stutzin et al., 1989). From the 27 cats tested, 85.2% were seropositive.
7.3.2.1 The development of T. gondii vaccinations for cats
There have been a number of attempts at developing a vaccine against T. gondii in cats.
Frenkel et al., (1991) used a live mutant strain “T-263” in kittens and found that oocyst
shedding was reduced by 84%. T-263 consists of live bradyzoites however and is a major
disadvantage using this approach. Freyre et al., (1993) further developed the experiments
and found that using two oral doses of the T-263 strain induced immunity to oocyst shedding.
Field trials of an oral cat vaccine using T-263 have been conducted and concluded that the
vaccine was effective (Mateus-Pinilla et al., 1999). A deterministic computer simulation
model was then used to assess the effect of a feline vaccine on the transmission of T. gondii
on a pig farm (Mateus-Pinilla et al., 2002). A surprising result was that the initial T. gondii
prevalence in cats had no effect on T. gondii prevalence in the finishing pigs. The simulation
supported the findings from the field trail in that although the vaccine was effective, it had
less impact than a decrease in the number of farm cats.
Omata et al. (1996) tested 60Co-irradiated tachyzoites vaccine in cats, although only 3 of the
14 cats did not shed oocysts. A DNA vaccine (expressing ROP2 protein) has also been tested
but had no effect in reducing oocyst shedding (Mishima et al., 2002).
A study only recently published (Garcia et al., in press) has evaluated a feline vaccine made
from crude rhoptry proteins of T. gondii with Quil-A (an adjuvant). Eleven domestic short
hair cats (5 – 8 months old) were divided into four groups. Group 1 (n=3) received 200µg of
rhoptry proteins with 20 µg of Quil-A. Group 2 (n=3) received phosphate buffer saline
(PBS) with Quil-A (20 µg) while Group 3 (n=3) and Group 4 (n=2) received only PBS.
Group 3 were unvaccinated but challenged while Group 4 were the unvaccinated and
unchallenged controls. The doses were administered by the intranasal route over day 0, 21
and 42 days. The total volume of inoculant was 200µL. Groups 1, 2 and 3 were exposed to
600 tissue cysts on day 51.
One of the three cats from the vaccinated group 1 shed oocysts, 4 days after challenge. All
animals from groups 2 and 3 shed oocysts while the control group 4 did not shed oocysts
throughout the experiment. In comparative terms, group 1 cats shed 89.3% and 90.8% less
oocysts then groups 3 and 4 respectively.
7.3.3
Risk communication
The New Zealand Food Safety Authority website has two risk communication publications
that give advice on toxoplasmosis;
Food safety in pregnancy:
http://www.nzfsa.govt.nz/consumers/food-safety-topics/foodborne-illnesses/pregnancy/
Food safety when you have low immunity:
http://www.nzfsa.govt.nz/consumers/food-safety-topics/foodborne-illnesses/lowimmunity/lowimmunity.pdf
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
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January 2008
The US Centres for Disease Control have published a range of material aimed at cat owners,
pregnant women, people with HIV/AIDS and for general information:
http://www.cdc.gov/ncidod/dpd/parasites/toxoplasmosis/toxoplasmosis_brochure_8.2004.pdf
http://www.cdc.gov/NCIDOD/dpd/parasites/toxoplasmosis/factsht_toxoplasmosis.htm
http://www.cdc.gov/NCIDOD/dpd/parasites/toxoplasmosis/ToxoWomen.pdf
http://www.cdc.gov/hiv/pubs/brochure/oi_toxo.htm
A study of toxoplasmosis-related knowledge and practices among 403 US pregnant women
(Jones et al., 2003b) found knowledge to be low: 48% had seen/heard information about the
disease, 7% were aware of being tested, 40% knew it was an infection while 21% believed it
was caused by a poison. The highest level of knowledge was for the risk of transmission
from cats; 61% responded that the organism is shed in infected cats faeces, 60% knew that
changing cat litter was a risk for transmission but only 30% were aware the organism may be
found in raw or undercooked meat.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
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January 2008
8
CONCLUSIONS
8.1
Description of Risks to New Zealand Consumers
8.1.1
Risks associated with red meat and meat products
Meat containing Toxoplasma cysts is regarded in Europe and the US as an important source
of infection for humans (the organism is not considered to be transmitted from person to
person).
Toxoplasmosis does not often cause serious disease in immunocompetent people. However,
the risk to immunocompromised people and the foetuses of pregnant women is considerable.
In the case of the foetus there is a high likelihood of serious long-term illness caused by
transmission of infection. Estimates of economic cost and disease burden for toxoplasmosis
have been significant, making the illness prominent amongst diseases which may be
foodborne.
The available data on seropositivity of the whole New Zealand population suggest that
infection with Toxoplasma is as prevalent in New Zealand as other developed countries.
Predictions of the incidence of symptomatic illness in New Zealand do not appear to be borne
out by actual observations. Studies of seroconversion in pregnant women in New Zealand
suggest a higher prevalence of congenital toxoplasmosis than has actually been observed, and
the study authors claim that these latter data argue against the need for antenatal screening.
In addition, the number of cases of diagnosed acquired toxoplasmosis in New Zealand
totalled 84 for the years 2000 to 2006. This is apparently lower than might be predicted from
the estimated 200 cases per year of ocular toxoplasmosis (only one of the outcomes of
acquired toxoplasmosis) reported for the Netherlands (population 16.5 million) (Kemmeren
et al., 2006).
While information on seropositivity in New Zealand livestock is limited, it is likely that New
Zealanders domestically produced red meat does contain Toxoplasma. Imported red meat is
less likely to contribute to exposure given that only small amounts of beef and sheep meat are
imported, and pigmeat is required to be frozen. Ameliorating factors for any exposure are
that animal seropositivity appears to overestimate infectivity, and Toxoplasma exposure will
be controlled through cooking and freezing.
Despite the focus on cats as the primary host, ownership of cats as pets has not always been
identified as a risk factor in case-control studies of pregnant women. These studies have
identified the consumption of undercooked meats as a risk factor, although the most recent
study, from England, did not.
The current shortage of information on the prevalence of infection in New Zealand livestock,
or the prevalence of contamination in red meat, precludes a definitive risk assessment of this
food/hazard combination. As noted by EFSA, considerable method development would be
required if efficient monitoring programmes for livestock or food were to be implemented.
Education programmes for vulnerable groups in relation to toxoplasmosis, as recommended
by EFSA, are in place in New Zealand.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
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January 2008
8.1.2
Risks associated with other foods
In addition to red meat sources, the organism has been found in chicken and pigeons (Smith,
1991) but no outbreaks or other evidence for transmission by these foods have been found.
Other vehicles associated with outbreaks have been unpasteurised goat’s milk (Skinner et al.,
1990; Sacks et al., 1982) ice-cream (linked to contaminated water) (de Moura et al., 2006)
and municipal water supplies (de Moura et al., 2006, Bowie et al., 1997).
Food contaminated with oocysts such as soil grown vegetables are another potential source of
infection, particularly where there is a population of cats (Smith, 1993).
8.1.3
Risk Assessment Options
Prevalence data on the presence of Toxoplasma cysts in red meat and meat products to
estimate the exposure of the New Zealand population are lacking, which precludes a
quantitative risk assessment.
8.2
Commentary on Risk Management Options
Decision making regarding risk management options must follow a better assessment of the
risk of foodborne transmission of this illness. Risk communication aimed at pregnant women
exist.
8.3
Data Gaps
The data gaps identified in this Risk Profile are:
•
•
•
•
•
Prevalence of Toxoplasma infection in livestock in New Zealand;
Prevalence of contamination of red meat and red meat products with T. gondii in New
Zealand;
Accurate data concerning toxoplasmosis cases in “at risk” groups;
Lack of data regarding prevalence of infection in domestic cats (the definitive host) in
New Zealand; and,
Information on awareness by at risk groups in relation to the transmission risks of T.
gondii, this information would be useful in targeting risk communication messages.
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
53
January 2008
9
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APPENDIX 1: CATEGORIES FOR RISK PROFILES
The assignment of a category for a food/hazard combination uses two criteria: incidence and
severity.
1. Incidence
The incidence is an estimate of the proportion of the foodborne disease rate due to an
individual hazard, that is transmitted by a single food or food group.
The overall rate of foodborne disease caused by individual hazards can be derived from
information in the published estimate of foodborne disease (Lake et al., 2000). This estimate
has been updated to reflect more recent notifications rates for the 12 months to June 2001,
but still using 1996 census figures (3,681,546 population). Rates include estimates for
unreported cases who do not present to a GP.
Disease/organism
Campylobacteriosis
Listeriosis
VTEC/STEC
Salmonellosis
Yersiniosis
Shigellosis
NLV*
Toxins*
Typhoid*
Hepatitis A*
* not recalculated.
Food rate (/100,000
population)
Calculated for 12 months to
June 2001
1320
0.4
1.9
176
38
7
478
414
0.3
0.4
Food rate (/100,000 population)
Calculated for 12 months to
December 1998
2047
0.4
1.4
230
62
7
478
414
0.3
0.4
These are total foodborne rates, so it is probably safe to assume that in most cases the rates
associated with a particular food are likely to be an order of magnitude lower. For instance, a
category of “>1000” would only be assigned if it was decided that all campylobacteriosis was
due to a single food/food type.
The following categories are proposed for the rates attributable to a single hazard/food (or
food group) combination:
Category
1
Rate range
>100
2
10-100
3
4
1-10
<1
Comments/examples
Significant contributor to foodborne campylobacteriosis
Major contributor to foodborne NLV
Major contributor to foodborne salmonellosis
Significant contributor to foodborne NLV
Major contributor to foodborne yersiniosis, shigellosis
Major contributor to foodborne listeriosis
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A further category, of “no evidence for foodborne disease in New Zealand” is desirable, but
it was considered more appropriate to make this separate from the others. Also separate is
another category, of “no information to determine level of foodborne disease in New
Zealand”.
The estimation of the proportion of the total foodborne disease rate contributed by a single
food or food group will require information from a variety of sources including:
•
•
•
exposure estimates
results from epidemiological studies (case control risk factors)
overseas estimates
For illnesses where the rate is <1 per 100,000 the ability to assign a proportion is unlikely to
be sensible. For such illnesses it may be more useful to consider a Risk Profile across the
range of all high risk foods, rather than individual foods or food groups.
2. Severity
Severity is related to the probability of severe outcomes from infection with the hazard. The
outcomes of infectious intestinal disease are defined in the estimate of the incidence (Lake et
al., 2000) as:
• death
• hospitalised and long term illness (GBS, reactive arthritis, HUS)
• hospitalised and recover
• visit a GP but not hospitalised
• do not visit a GP
The first three categories of cases were classed as severe outcomes. Some hospitalisations
will result from dehydration, etc. caused by gastrointestinal disease. However, for infections
with Listeria and STEC hospitalisation will result from more severe illness, even if recovery
is achieved. The proportion of severe outcomes resulting from infection with the hazards can
be estimated from the proportion of cases hospitalised and recover, hospitalised and long
term illness, and deaths (Lake et al., 2000).
Disease/organism
Campylobacteriosis
Listeriosis
VTEC/STEC
Salmonellosis
Yersiniosis
Shigellosis
NLV
Hepatitis A
Typhoid
Toxins
Percentage of outcomes involving death or long term illness
from foodborne cases
0.3
60.0
10.4
1.0
0.4
2.7
Assumed to be <0.5%
15.4
83.3
Assumed to be <0.5%
Categories for the probability of severe outcomes are suggested as follows:
Risk Profile: Toxoplasma gondii in Red Meat
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January 2008
Severity
Category
1
2
3
Percentage of cases that
experience severe outcomes
>5%
0.5 – 5%
<0.5%
Examples
listeriosis, STEC, hepatitis A, typhoid
salmonellosis, shigellosis
campylobacteriosis, yersiniosis, NLV, toxins
There are a number of hazards for which the incidence of foodborne disease is uncertain.
These have been assigned to the above severity categories as follows:
Severity category 1:
Bacteria
Clostridium botulinum
Protozoa
Toxoplasma
Severity category 3:
Bacteria
Aeromonas/Plesiomonas
Arcobacter
E. coli (pathogenic, other than STEC)
Pseudomonas
Streptococcus
Vibrio parahaemolyticus
Viruses
Others (e.g. rotavirus)
Protozoa
Giardia
Cryptosporidium
Cyclospora
Others (e.g. Entamoeba)
Risk Profile: Toxoplasma gondii in Red Meat
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January 2008
Proposed Category Matrix
Incidence
Severity 1
Severity 2
Severity 3
>100
10-100
1-10
<1
Alternatives:
No evidence for foodborne disease in New Zealand
No information to determine level of foodborne disease in New Zealand
Risk Profile: Toxoplasma gondii in Red Meat
and Meat Products
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January 2008